Inflammation Plays Role in Starting, Stopping Cancer- (HealthDay News-20/09/2004)

A new strategy for cancer therapy, which converts the tumor-promoting effect of the immune system's inflammatory response into a cancer-killing outcome, is suggested in research findings by investigators at the University of California, San Diego (UCSD) School of Medicine. The findings provide new insight into the immune system's response to inflammation, the connection between inflammation and malignancy, and how the delicate balance between cancer promotion and inhibition can be manipulated in the patient's favor, according to the study's senior author, Michael Karin, Ph.D., UCSD professor of pharmacology, American Cancer Society Research Professor, and a member of the Rebecca and John Moores UCSD Cancer Center.

The studies in mice with colon or breast cancer showed that cancer metastasis, the growth of malignant tumors beyond the original site, was halted with inhibition of either one of two naturally occurring substances, a pro-inflammatory protein called nuclear factor-kappa B (NF-kB) or an inflammatory mediator called tumor necrosis factor alpha (TNFα). The result, published in the September 20, 2004 issue of the journal Cancer Cell, was increased effectiveness of a cancer-killing protein called TNF-related apoptosis-inducing ligand (TRAIL), leading to a decrease in cancer cells and increase in the life span of tumor-bearing mice. The study's first author, Jun-Li Luo, M.D., Ph.D., a member of the Karin team in the UCSD Laboratory of Gene Regulation and Signal Transduction, explained that normally, inflammation associated with malignancy activates NF-kB, TNFα and TRAIL, all at the same time. However, NF-kB has the upper hand, and with TNFα, stimulates tumor growth faster than TRAIL can inhibit it.

"Our results suggest that is it possible to use NF-kB or TNFα inhibitors to prevent inflammation-induced tumor growth, thus destroying their advantage, and allowing TRAIL to tip the balance in its favor," Luo said.

The study builds upon previous work in the Karin lab recently featured as the cover article in the August 6, 2004 issue of the journal Cell*. In that study, the researchers provided the first evidence of the molecular link between inflammation and cancer. They determined that an enzyme called I-kappa-B kinase beta (IKKβ) is required for the activation of NF-kB, which acts as a master switch to turn on inflammation in response to bacterial or viral infections. In turn, NF-kB sets off a chain of reactions that lead to cancer.

Mice used in the new study were given colon or breast tumor cells which metastasized to the lung. Some of these cancer cells served as "controls," while other cells were given a protein that specifically inhibited activation of NF-kB, only in cancer cells. The different cells were injected into mice and all were able to establish metastatic growth in the lung, regardless of their ability or inability to activate NF-kB. After a week, all mice were injected with bacterial lipopolysaccchide (LPS), which induced inflammation. A post-mortum inspection of the mice showed that following inflammation, the control cells formed more numerous and larger tumor nodules, while the tumors formed by cells in which NF-kB was inhibited, had shrunk or partially disappeared after the LPS injection. As a result, mice injected with cancer cells lacking NF-kB activity exhibited much better survival than mice inoculated with control cells.

In further tests to determine how NF-kB activation mediates inflammation-induced tumor growth, the team studied mouse lung tissue as well as tumor nodules for expression of specific proteins known to modulate the body's normal cell-killing process. Death-inhibiting proteins were abundant in tumors formed by cancer cells with normal NF-kB, but were absent in the tumors formed by cancer cells where NF-kB was inhibited. While NF-kB is known to convert inflammatory stimuli into tumor growth signals, it is also known to activate TNFα, a major proinflammatory protein initially thought to play a role in the death of cancer cells. Investigators first reasoned that TNFα might be responsible for the death of cancer cells in which NF-kB was inhibited, seen in this study, since previous experiments have shown that high doses of TNFα can kill tumor cells when NF-kB activity is inhibited.

However, further experiments proved otherwise. When inflammation-inducing LPS was administered to tumor-bearing mice with normal NF-kB, the result was a rapid and robust induction of circulating TNFα and eventual acceleration of cancer growth. However, administration of an anti-TNFα antibody five minutes after LPS challenge neutralized most of the circulating TNFα, inhibited NF-kB activation in cancer cells, and prevented the inflammation-induced acceleration of tumor growth. Rather than TNFα, the team found that TRAIL, a member of the TNF superfamily and a relative of TNFα, was the specific protein responsible for the tumor death response. While both NF-kB and TRAIL are activated in response to inflammation, NF-kB takes control, inhibits cell death and promotes cancer growth. When NF-kB or TNFα were inhibited, however, TRAIL was able to strongly assert its ability to reduce tumor growth by killing cancer cells. The role of TRAIL was further illustrated in additional experiments where a neutralizing anti-TRAIL antibody was injected into the mice following the LPS challenge. The result was tumor growth.

In their summary, the researchers said that since TNFα does not make a major contribution to tumor killing and instead may promote tumor growth, it may be advisable to develop drugs which reduce inflammation-associated toxicities, block inflammation-induced tumor growth and clear the way for TRAIL to initiate tumor killing. The latter approach can be accomplished by the use of NF-kB inhibitors, together with anti-TNFα drugs, the researchers contend. These drugs should be used in combination with TRAIL or TRAIL-inducing cytokines, such as beta interferon. 

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Cancer survivors' comorbid conditions often ignored-(NT Online Clinical News- 14/09/2004)

Cancer survivors often miss out on care for unrelated conditions such as heart disease and diabetes, according to new research. The authors of a report published online by the journal Cancer September 13th online issue of Cancer. Specialists say: 'For several years after treatment, the patient is mostly focused on 'will my cancer come back?' and they're not getting their lipids checked and those sorts of things.'

Their findings are based on an analysis of nearly 15,000 subjects who had survived at least 5 years after being diagnosed with nonmetastatic colorectal cancer. Compared with controls, cancer survivors were less likely to receive preventative services as well as recommended care for a variety of chronic and acute conditions and were at risk for not receiving appropriate follow-up for heart failure and diabetes care. Survivors were 19% less likely to receive recommended care for chronic medical conditions than control subjects. 'It's important to raise awareness of this issue so that we, as oncologists, discuss with our patients the need for follow-up with a primary care physician after their cancer treatment is completed. We don't want to cure their cancer and then have them die from other things,' say the authors.

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IBD (Crohn's, Colitis) 'joins' cancer, anti-inflammatory diseases in associated blood vessel growth-(Yahoo News-13/09/2004)

Over at least the last decade it has been recognized that the growth of new blood vessels is critical in the pathogenesis of cancer because it increases blood supply to malignant tissue. Relatively recently, a novel pathogenic role of angiogenesis has been established for such chronic inflammatory diseases as rheumatoid arthritis, psoriasis and atherosclerosis. As a result, suppressing neoangiogenesis is being investigated as a therapeutic approach for not only cancer, but also chronic inflammation. Whether neoangiogenesis also occurs in Crohn's Disease (CD) and ulcerative colitis (UC), the major constituents of Inflammatory Bowel Diseases (IBD), has never been studied, according to the authors of a paper presented at an IBD translational conference sponsored by the American Physiological Society.

The paper is entitled, "Neoangiogenesis: a new component in Inflammatory Bowel Diseases pathogenesis." Lead author Silvio Danese of Case Western Reserve University School of Medicine and Universita' Cattolica del S. Cuore, Rome, Italy, collaborated with colleagues Miquel Sans, Brenda Reyes-Rivera, Gail West, Homa Phillips, Joe Willis and Claudio Fiocchi at Case Western Reserve University School of Medicine; Carol de la Motte at the Cleveland Clinic Foundation; and Roberto Pola and Antonio Gasbarrini at Universita' Cattolica del S. Cuore.

According to Danese, "Our results show that increased vascularization is present in IBD, and the inflamed mucosal microenvironment actively promotes angiogenesis." Furthermore, he said that "the intestinal microvascularization of both CD and UC displays an activated profile as shown by the expression of angiogenic marker áVâ3 integrin. "Targeting this integrin could be a potential therapeutic approach for IBD," similar to approaches in other forms of chronic inflammation, Danese said. "These results provide the initial material and conceptual framework for investigating angiogenesis in IBD both as a pathogenic component as well as a possible therapeutic target," he added.

The researchers took normal control and actively involved IBD colonic mucosa and immunostained them for the endothelial antigen CD31. Vessels were quantified by digital morphometry (vessel density/field). Microvessel áVâ3 expression was studied in vivo by confocal microscopy, and in vitro by flow cytometric analysis of human intestinal microvascular endothelial cells (HIMEC) activated by bFGF, VEGF and TNF-á. Pro-angiogenic bioactivity of mucosal extracts was tested in vitro by induction of HIMEC migration (cells/field) and in vivo by the mouse corneal angiogenesis assay.

They found that microvessel density was significantly higher in CD and UC compared with control mucosa. áVâ3 expression was only sporadically detected in normal mucosa, whereas it was ubiquitously and strongly expressed in IBD microvasculature as confirmed by co-localization with CD31. The expression of áVâ3 by HIMEC was upregulated by bFGF and TNF-á but not VEGF, and its targeting with a specific antibody (Vitaxin) induced marked HIMEC apoptosis. HIMEC migration was dose-dependently induced by both CD and UC mucosal extracts, and was significantly greater than that induced by control extracts, the researchers reported. As shown by neutralizing antibodies, migration was primarily dependent on IL-8, and less on bFGF or VEGF. Finally, IBD-derived extracts induced a potent angiogenic response in the corneal assay compared to control-derived extracts, they noted.

The results provide "morphological and functional evidence of strong pro-angiogenic activity in both CD and UC mucosa, indicating that the local microvasculature undergoes an intense process of neoangiogenesis in IBD," the paper said. The authors said this "suggests that neoangiogenesis is a vital component of IBD pathogenesis, and provides the material and conceptual framework for considering anti-angiogenic therapies for IBD as is currently ongoing in other autoimmune disorders."

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Hypnosis 'reduces cancer pain'-(Yahoo News-09/09/2004)

Childhood cancer patients suffer less pain when placed under hypnosis, scientists have claimed. Children who had been hypnotised in trials reported they had less pain from medical procedures as well as cancer-related pain. Dr Christina Liossi, from University of Wales, Swansea, suggested there was even tentative evidence that hypnosis prolonged the lives of cancer patients. The research is being presented at the BA Festival of Science in Exeter.

In one study, 80 children were placed in four groups: two experimental groups who were treated with an anaesthetic and hypnosis. Two control groups were just given the anaesthetic. "All [40] children who used hypnosis with a local anaesthetic felt much less pain than children who were just given the local anaesthetic," said Dr Liossi.

The children, aged six to 16, were placed under hypnosis by experts and then taught to hypnotise themselves before they underwent procedures. Children not treated with hypnosis were talked to and counselled instead. "We asked children to rate their pain from 0 to 5 on a graded scale. Before we perform hypnosis we ask them to rate their pain on this scale," Dr Liossi explained. "Then we introduce hypnosis and then we ask them to rate pain again and they report much less."

Other evidence presented at the festival also supports the idea that hypnosis is a genuine physical state and that people are not simply deceiving themselves into thinking they are hypnotised. Individuals who are highly susceptible to being placed under hypnosis show that there are changes in the left frontal cortex of the brain and a structure called the cingulated gyrus when viewed through a functional MRI (magnetic resonance imaging) scanner.

"The frontal lobe is concerned with our planning, our future actions, our analysis of the here and now, our critical evaluation and the things we do so we don't make silly mistakes," said Dr John Gruzelier of Imperial College, London. "If you think about what the hypnotist does, he asks you to go with the flow and not critically analyse what you're doing." Dr Liossi suggested there was even evidence that hypnosis might prolong life in adult cancer patients. "There are some studies and there are some encouraging results from these," she said. 

Adult cancer patients placed under hypnosis show fewer cancer-related symptoms such as nausea, vomiting and pain, said Dr Liossi. "There are some studies and there are some encouraging results from these that hypnosis can probably improve the survival of cancer patients. But at the moment there isn't enough evidence."

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Cancer Patients Expect Many Treatment Side Effects-(Reuters Health-03/09/2004)

People facing the prospect of cancer treatment typically expect to suffer numerous side effects -- often more than is actually likely -- a study suggests. The survey of 938 cancer patients found that when asked about 12 potential side effects of treatment such as fatigue, nausea and hair loss, patients said they expected to suffer nine of them, on average. Women and patients younger than 60 were particularly likely to expect a high number of side effects. That patients typically expected so many side effects came as a surprise, according to lead study author Maarten Hofman, a researcher at the University of Rochester Cancer Center in Rochester, New York.

It means that many patients may believe they're destined for more treatment-related problems than they are likely to have, he told Reuters Health. This is important, according to Hofman, because there's evidence that expecting to have a side effect makes it more likely to become a reality. For example, he noted, some studies suggest that people who expect cancer treatment to nauseate them are indeed more likely to suffer nausea. Whether the same might be true of other treatment-related symptoms is unknown, and Hofman said more research is needed into the question of how expectations sway actual experience. It's "probably better," he added, for cancer patients' expectations to be in line with what they're likely to face.

The current study, reported in the journal Cancer, involved patients from 17 oncology practices who answered questions about symptoms they had prior to treatment, and the symptoms they expected to have once they started therapy. Nearly all patients expected to suffer fatigue during treatment, and 70 percent or more believed they would have to deal with nausea, sleep disturbances, weight and hair loss, skin problems, depression and pain. Overall, women and younger patients expected more side effects than did men and patients older than 60. If research can paint a "profile" of the patients most likely to have a dim view of how they'll fare during treatment, according to Hofman, doctors could pay particular attention to the side-effect concerns of those patients.

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Too Much Radiation From Full-Body CT Scans?-(Yahoo News-31/08/2004)

They promise to cut your risk of dying from cancer. Yet full-body CT scans themselves pose a real cancer risk, new calculations suggest. X-rays from a single full-body CT scan give a dose of radiation similar to cancer-associated radiation doses in A-bomb survivors, finds David J. Brenner, PhD, director of Columbia University's center for radiological research. It's not a huge risk, especially for someone with symptoms of a dangerous condition. But when used to screen healthy people for hidden evidence of disease, the risk may outweigh the benefit. And if a healthy person gets repeated full-body scans, cancer risks multiply, Brenner and colleague Carl D. Elliston report in the September issue of Radiology.

"The risks from a single full-body CT scan are not large: If 1,200 45-year-old people got one, you might expect one to die from radiation-induced cancer," Brenner tells WebMD. "But if you are thinking of doing this on a regular basis, as a routine screening modality, then the radiation doses start to add up and the risks then start to get quite high." A single full-body CT scan gives a person a total radiation dose of about 12 mSv. That's close to the 20-mSv dose linked to cancer in Japanese survivors of atomic bombs. And each of these scans adds another 12 mSv to a person's total lifetime exposure. An mSv is a unit for measuring radiation dose.

Studies suggest that full-body CT scans aren't likely to benefit anybody under the age of 45. This led Brenner to calculate cancer risk for someone who decided to have annual full-body CT scans beginning at that time. "If you start at age 45, and have them annually until you are 75, you are talking about a one-in-50 chance of radiation-induced cancer, which is a huge risk," Brenner says. "Until the benefit is clear, there is not much of an advantage to having routine body scans yearly or even every two years. But a single scan is not much of an issue."

For several years now, freestanding clinics have been offering full-body CT scans to anyone who wants one. Ads for the clinics promise early detection of dangerous diseases such as cancer and heart disease. The idea is that full-body CT scans will find tumors other signs of disease in their earliest, most treatable stages -- before a person has any symptoms of illness.

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Cancer Can Ruin a Life, Even if You Survive -- Study-(Reuters-31/08/2004)

Cancer can really mess up a person's life, even years after he or she has beaten the disease, U.S. researchers reported on Tuesday. Cancer survivors have poorer health, lose more days from work and have a generally lower quality of life than people who have never had cancer, the study in the Journal of the National Cancer Institute estimates that 9.8 million cancer patients and survivors are alive now in the United States. About 64 percent of adults and 79 percent of children now survive cancer for at least five years, the CDC says.

These patients have not been studied much, but a series of reports have called for better coordination of care for cancer survivors, especially children. They have found that the harsh treatments often needed to beat cancer, including surgery, chemotherapy and radiation, can themselves have lasting effects on health. Robin Yabroff of the National Cancer Institute and colleagues at the Agency for Healthcare Research and Quality studied a questionnaire of 1,800 cancer survivors and nearly 5,500 people who never had cancer and matched for age, sex, and level of education.

They found that 31 percent of cancer survivors reported having fair or poor health, compared to 18 percent of people who never had cancer. Only 13 percent of cancer survivors described their health as "excellent," compared to 21.9 percent of non-patients, although a similar percentage described their health as "good" -- 33 percent of cancer survivors and 29 percent of non-patients. "Survivors were more likely to have spent 10 or more days in bed in the past 12 months than control subjects (14 percent versus 7.7 percent)," the researchers wrote. Cancer survivors were also more likely than control subjects to report limitations with arthritis or rheumatism, back or neck problems, fractures or bone or joint injuries, hypertension, or lung or breath problems than control subjects," they added.

But cancer survivors were no more likely to have heart problems, stroke, diabetes, depression, anxiety or other emotional problems, the survey found. The study included a range of cancer patients, including 16 percent who had only been diagnosed in the past year, 19 percent within 6 to 10 years and 27 percent who had survived 11 or more years.

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Scientists Establish Database of Genes Associated With Cancer Drug Resistance-(Yahoo News-24/08/2004)

Scientists at the National Cancer Institute (NCI), a part of the National Institutes of Health, have created a database of information about a group of genes associated with multidrug resistance in cancerous tumors. The research, published in the August 24, 2004, issue of Cancer Cell*, details the gene expression of a 48-member family of proteins called ABC transporters. The NCI scientists identified associations between expression of individual ABC transporters in cancer cells and resistance to specific drugs. Though ABC transporters are primarily associated with drug resistance, the researchers report an association between some of these proteins and an increase in effectiveness of some cancer drugs. Their database should serve as a starting point for research into novel therapies designed either to evade or exploit the action of ABC transporters.

ABC transport proteins are embedded in the cell membrane and regulate traffic of many molecules, including hormones, lipids, and drugs, in and out of the cell. Because they transport toxic materials out of cells, many of these 48 proteins confer resistance to cancer drugs in humans. The study's lead authors were Jean-Philippe Annereau, Ph.D., and Gergely Szakács, M.D., Ph.D., both visiting fellows at NCI's Center for Cancer Research (CCR). Szakács said, "Multidrug resistance is a major barrier to effective cancer chemotherapy, and even low levels of resistance can have a significant impact on the efficacy of chemotherapy."

Though these proteins have major implications for the treatment of cancer, previous studies had characterized only 17 of them using much less sensitive techniques. Szakács and Annereau studied the ABC transporters in a group of cancer cell lines called the NCI-60 cells, which includes leukemias, melanomas, and ovarian, breast, prostate, lung, renal, and colon cancers.

They used real-time polymerase chain reaction to detect and quantify the expression of ABC transporter genes as messenger RNA in these cells. With help from collaborators in the laboratory of John Weinstein, M.D., Ph.D., also in CCR, the researchers found statistical correlations between tests of the cell lines' sensitivity to cancer drugs and these cells' expression of ABC transporters. Further tests, such as measuring changes in cell growth to evaluate the cells' response to the drugs, supported the statistical correlations.

Analysis of 68,592 ABC gene and drug relationships yielded 131 strongly inverse-correlated pairs--that is, in these 131 cases, cells' ABC gene expression was strongly correlated with decreased sensitivity to the drug. According to Michael Gottesman, M.D., one of the paper's senior authors and chief of the Laboratory of Cell Biology in CCR, "These results indicate that some of the ABC transporters whose function remains unknown can influence the response of cells to cancer treatment."

Gottesman, Szakács, and colleagues hope this data will be used to find commonalities in compounds transported by MDR1, one of the ABC proteins most strongly associated with multidrug resistance. With this information, they could begin developing a drug to undermine MDR1's ability to transport drugs out of the cell.

Expression of some ABC transporters, most notably MDR1, caused an increase in cancer cells' sensitivity to some drugs. This increase was unexpected, as MDR1 is perhaps the best-known multidrug resistance protein. The researchers advocate further research in order to discover additional compounds that interact in this way with MDR1 and other ABC transporters.

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Some Programs To Increase Exercise Have Lasting Effects-(Yahoo News-13/08/2004)

Some behavior modification programs designed to increase exercise show continued effects for at least 3 months after they end, according to a new report released by the Agency for Healthcare Research and Quality and supported by the National Cancer Institute (NCI), part of the National Institutes of Health. However, the review of existing evidence also demonstrated that it is difficult to achieve sustainable gains in increased physical activity because few studies looked at the effects of these programs for more than 1 year. "This report underscores that the successful expansion of efforts to increase physical activity first requires a better understanding of what makes programs effective," said Health and Human Services Secretary Tommy G. Thompson.

In addition to reviewing evidence from physical activity interventions in healthy populations, the authors also examined the effects of exercise on cancer survivors—people living with cancer or those who have a personal history of the disease. The report concluded that exercise programs can improve cancer patients' functional capacity and cardiopulmonary fitness, reduce symptoms of fatigue, and improve quality of life during and after cancer treatment. In addition, exercise can reduce cancer patients' symptoms of anxiety, depression during treatment. The report suggests that physical activity may have other positive effects among cancer patients, but at this time there are too few studies to reach any conclusions.

NCI Director Andrew C. von Eschenbach, M.D., said, "Regular physical activity is important for both lowering the risk for and managing multiple diseases, including some cancers. The more we understand about how to help people start and maintain exercise programs, the more we can help cancer survivors combat some of the early and late effects of cancer and its treatment."

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Daffodils help fund cancer research-(Yahoo News-17/08/2004)

Ten years, 10 children and $1.2 million - this Friday's Daffodil Day marks the 10th birthday of the Cancer Council of Tasmania's major, yearly fund-raiser. Yesterday, 10 youngsters from grade 3-4 at St Leonards Primary School became the symbol for the day that organisers hope will pump $205,000 into the council's Tasmanian coffers. Regional services officer for the council in the North Jennifer Lyall said that the children highlight a generation who were not afraid to ask questions about cancer, once a taboo subject. 

"Each child represents a year that the day has been running in Tasmania. Due to continuous improvements in research and treatment, one third of all cancers are now preventable and more than half of all cancers are successfully treated," Mrs Lyall said. "Between 1995 and 2003, community support of Daffodil Day in Tasmania has raised over $1.2 million." One in three Tasmanians have a chance of being diagnosed with cancer in their lifetime and those not diagnosed will be impacted indirectly by a friend or family member who is, Mrs Lyall said. "It is worth noting that 15 per cent of all new cancers diagnosed between 1980 and 1999 were attributed to smoking related cancers," she said.

This year's Daffodil Day merchandise includes a yellow soft football, Dougal and Daffodil Day bear, and a range of ribbons, lapel pins and pens.  

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Doctor's cancer cure challenged-(Yahoo News-16/08/2004)

Australia's peak radiology body is seeking to settle a 30-year argument with a Perth-based surgeon about his controversial cancer treatment once and for all. Dr John Holt, 79, claims to have successfully treated thousands of cancer patients with injections of glucose-blocking agent and high-frequency radio-wave treatments, administered by the German-invented Tronado machine. Dr Holt, a former director of West Australia's Institute of Radiotherapy and Oncology, believes cancer cells are electronically different to normal cells and that cancer is a disease of defective glucose metabolism. But the medical fraternity has largely rejected his theories because of a lack of scientific evidence that the treatment works – separate from patient testimonials that have frequently been aired in national media.

Royal Australian and New Zealand College of Radiologists dean of radiation oncology Professor Lester Peters yesterday said he would write to Dr Holt offering to set up an independent committee to review his patient files and success rates over the past 30 years, to determine if a large clinical trial was justified. "If there is any basis to it, it is very much in our interest (to investigate)," he said. Professor Peters said Dr Holt has not published results in respected medical journals, performed clinical trials or submitted his therapy to independent scrutiny. He said a National Health and Medical Research Council review 20 years ago found no benefit in the treatment, and a small clinical trial done by the Cancer Council of Western Australia found it was no more beneficial than traditional treatment. "When you just hear testimonials from people, you get some idea of those who have improved but you have no idea of the proportion (of patients) that did not improve," Professor Peters said. "Dead people don't give testimonials."

Professor Peters said there was no allegation Dr Holt was "ripping people off" but his methods would not gain any credibility by remaining a secret or untested. "If he's on to something, wouldn't he want to train some new young blood to follow on. If he says 'no one believes me, why bother publishing it', it's a self-fulfilling prophecy – of course, no one is going to believe him." Dr Holt could not be contacted yesterday. Queensland Cancer Fund medical and scientific committee chair Associate Professor Euan Walpole said any medical treatment had to be based on benefit proven through strict, scientific research that could be subjected to outside scrutiny.

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Cancer cells destroyed by designer virus that leaves good cells alone-(Yahoo News-25/07/2004)

A team of scientists at Cancer Research UK have created a virus that targets and destroys cancer cells while leaving good cells alone. They say the cancer cells selfish survival instinct is the reason this new breakthrough works. Cancer cells do not shut down when they are infected with this virus. Normal cells, on the other hand, do shut down. You can read about this latest research in the journal Molecular Therapy. A virus is a good way of carrying anti-cancer treatment straight into a cell. A virus has the ability to enter cells undetected. The problem for scientists has always been being able to enter just the cancer cells and not the good ones. This team of scientists, from Bart’s, Queen Mary’s School of Medicine and Dentistry, UK, have managed to engineer a virus that enters only the cancer cells.

They took out a gene from the virus which enables it to enter all cells by stealth. When this virus tries to enter a normal cell, it is detected and the cell destroys itself. This ‘suicide’ of the good cell prevents the infection and duplication of bad cells. A cancer cell, on the other hand, does not have this self-destruct button, it wants to survive at all costs. This is great because the virus enters it and replicates within the cancer cells. The replication allows the virus to spread throughout the tumour tissue, leading to the potential destruction of the tumour if toxins are placed in the virus. Scientists found that the virus spread through the cancer cells like wild fire but left the good cells alone. One of the problems with current chemotherapy is that it is not so targeted, a lot of good cells are destroyed, leaving patients debilitated.

With such good targeting, the scientists say it will become much easier to have highly selective anti cancer treatment. The scientists plan to place a toxic gene into the virus so that the toxin can destroy the cancer cells. As the cancer will make more copies of the virus anyway, not that many copies of the virus will be needed initially for effective treatment. The cancer cell does all the hard work by creating more and more copies of the virus, said Professor Lemoine, lead scientist. When the new treatment becomes available the virus will be injected into the bloodstream, rather than straight into the tumour. If all goes well, clinical trials should start next year.

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The Body, Not the Mind, Predicts Cancer Survival- (HealthDayNews-26/07/2004)

Terminal cancer patients may feel anxious or spiritually distressed, but their physical symptoms - not their emotions - are what signal the beginning of the end, an international research team reports. In the early stages of terminal cancer, patients with intense nausea are 70 percent more likely to die within six months than patients without that symptom, researchers report in the July 26 online edition of Cancer. In late-stage cancer, shortness of breath was associated with a 50 percent increase in patients' immediate risk of dying, they found. These physical symptoms appear to reflect the severity of a patient's cancer cachexia, a wasting syndrome that causes people with tumors to become anorexic, weak and fatigued.

"The presence of these symptoms should be like red flags," indicating that a patient's cancer is more advanced than it might otherwise appear, explained study author Dr. Antonio Vigano, an assistant professor in the Palliative Care Division of McGill University Health Center in Montreal. "I think that patients presented with these symptoms should be referred earlier to palliative care, and treatment to improve the symptoms should be started earlier rather than later," he said.

The study is important because it scientifically supports what health professionals who work with advanced cancer patients already know, said Dr. Robert A. Brescia, director of the Palliative Care Institute at Calvary Hospital in the Bronx, which provides end-of-life care to adults with advanced cancer. "Cancer patients often suffer increasing physical distress -- including shortness of breath, weakness, nausea and vomiting -- as they get closer to death," he noted. Nevertheless, Brescia cautions against focusing on risk of death in dealing with patients and their families. "It is very risky, and often inappropriate, to try and predict how long any particular patient has to live," he asserted. "Even the most experienced clinicians will tell you that this is difficult to do, and attempting to do so can unwittingly add to the suffering of both the patient and family."

Existing research suggests that patients' physical symptoms, not their emotions, are good predictors of how long they will live. But because those studies failed to use precise research methods, the results were questionable. To clarify the issue, Vigano and colleagues studied two groups of terminal cancer patients at different stages of the disease. One group included 248 patients admitted to Cross Cancer Institute in Edmonton, Alberta, at the onset of terminal cancer. The other group represented 756 new referrals to palliative home-care services in Southern Ireland; these people were cared for in the later stages of their disease. Investigators examined the relationship between how long the patients lived and various quality-of-life measures, including physical and emotional symptoms. At each stage of the disease, physical factors predicted shorter survival.

For patients in the early stages of terminal cancer, risk of death increased 68 with nausea or vomiting and 28 percent with shortness of breath. But these associations were not as strong as other disease-related factors. For example, the risk of dying almost tripled for patients with liver metastases -- malignant tumors that originated elsewhere in the body and spread to the liver through the bloodstream. Death risk doubled for patients with high tumor burden, a measure that approximates the number of tumors they have, including primary tumors and secondary tumors that form as the cancer spreads. Among later-stage cancer patients, weakness, meaning a general lack of energy, boosted chances of dying by three, four and five times, respectively, for people with late-stage colorectal, genitourinary (including bladder, uterine, kidney, and prostate cancers) and breast cancer. If health-care providers are able to identify these symptoms, they can intervene in a way that will improve cancer patients' quality of life, Vigano said. 

Although anxiety and spiritual distress were not predictors of survival, Brescia nevertheless favors aggressively treating patients' psychological symptoms. "These symptoms often cause the patient and family even more pain and suffering than physical symptoms and too often are completely ignored by health-care professionals," he explained. 

In a separate study in the same edition of Cancer, Dr. Gopal K. Singh and colleagues from the National Cancer Institute report a link between income and education in cervical cancer patients. The study shows that the incidence and death rates for cervical cancer rose with increasing poverty and decreasing education levels.

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Research Discovery May Increase Effectiveness of Monoclonal Antibody Therapies for Cancer Recruitment of Innate Immune Cells Provides Additional Killing Mechanism-(PRNewswire-15/07/2004)

Researchers have identified a natural carbohydrate that recruits innate immune cells to assist monoclonal antibodies in the killing of cancer cells, providing a third mechanism by which this immunotherapy destroys tumors. The results were published in today's issue of The Journal of Immunology, the official publication of the American Association of Immunologists. An abstract of the article is available at http://www.jimmunol.org . Monoclonal antibodies, which are manufactured in a lab to target specific antigens present on tumor surfaces, are known to kill cancer cells two ways. One method is to attract Natural Killer and other cells to attack the tumor, a process also known as Antibody-Dependent Cellular Cytotoxicity (ADCC). The other method is to activate the complement system, a series of blood proteins that work together to puncture the tumor cells and destroy them (Complement- Dependent Cytotoxicity or CDC). A third killing mechanism, discovered by researchers at the James Graham Brown Cancer Center at the University of Louisville, relies on an orally administered yeast beta 1,3/1,6 glucan called WGP(R) Beta Glucan.

This natural carbohydrate binds to specific receptors on neutrophils, the most abundant immune cell in the body. The binding enables the neutrophils, which are not normally engaged in the fight against cancer, to "see" the cancer as foreign. The antibodies and complement attract the primed neutrophils to the site of the cancer where it joins the attack. In a recent study, 100 percent of mice with liver cancer that were treated with WGP Beta Glucan three days before the start of monoclonal antibody therapy survived 100 days, compared with only 35 days for mice treated with monoclonal antibodies only. Researchers observed significant increases in tumor regression in mice treated with WGP Beta Glucan in combination with Herceptin(R), a monoclonal antibody developed to treat metastatic breast cancer. "Our research over the past decade has firmly established the efficacy of beta glucan as an immune system enhancer and more recently as a highly promising complementary cancer immunotherapy," said Gordon Ross, Ph.D., lead researcher and Director of the Tumor Immunobiology Program at the James Graham Brown Cancer Center. "The next steps will be to study the benefits of WGP Beta Glucan in combination with monoclonal antibodies and cancer vaccines in humans."

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Bangladesh gets cancer hospital-(Yahoo News-10/07/2004)

Bangladeshi Prime Minister Khaleda Zia will lay the foundation of the nation's first fully-fledged cancer hospital in the capital, Dhaka. The country has an estimated one million cancer patients and about 150,000 die each year. According to medical experts, only 2% of patients have access to cancer units around the country. The new $15m hospital will have an initial 160 beds, rising to 500 by the year 2007. Experts say that every year, another 200,000 people develop some form of cancer - mostly lung cancer and leukaemia. Most patients die without being properly diagnosed or receiving adequate medical treatment. So the Dhaka Ahsania Mission undertook a project to set up the modern hospital in Dhaka. "We aim to provide quality treatment to cancer patients, especially the poor ones," said Kazi Rafiqul Alam of the non-governmental organisation. The hospital will have the latest technology, including medical, surgical and radiation oncology as well as a diagnostic centre for histopathology, endoscopy, colonoscopy and bronchoscopy.

Mr Alam said Bangladesh had no cancer hospital with the necessary equipment, except for the National Cancer Research Institute, which could treat only 50 patients at a time. The affluent go to India and other south-east Asian countries for treatment. "Cancer patients spend an estimated $83m annually for treatment abroad due to inadequate facilities in the country," Mr Alam said. The cost for treatment in the Ahsania Mission hospital will be 20% less than any cancer hospital in India, he said. The NGO has already started collecting money for the hospital through contributions from the public. It launched an appeal through two national newspapers a few months back.

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One in ten cancer patients die of severe sepsis-(Yahoo News-05/07/2004)

According to a research conducted by Eli Lilly & Co in Indianapolis, and Health Process Management, LLC, Pennsylvania, cancer patients who are admitted to hospitals contract severe sepsis, a disease which injures critical organs like the lungs and the kidneys, and causes death in almost ten per cent of the patients. Cancer patients are more susceptible to the disease as they become immuno-suppressed and their ability to fight off infection deteriorates. "Our study demonstrates the devastating complication of severe infections in cancer patients. Improvement in infection control, such as early appropriate antibiotics, in this population could have a significant impact on overall cancer survival," said Mark Williams, the author of the study. In general, cancer patients are nearly four times as likely to be hospitalized with severe sepsis than people without cancer. Patients suffering from lymphoma, leukemia or other blood cancers were even more susceptible to severe sepsis than those suffering from cancer of a solid organ.

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Diabetes appears to increase the risk of death from a number of types of cancer-(Yahoo News-04/07/2004)

Diabetes appears to increase the risk of death from a number of types of cancer, new research suggests. Moreover, this holds true even after accounting for obesity, which is common among diabetics and is a well-known risk factor for cancer. "Several studies have suggested that diabetes mellitus may alter the risk of developing a variety of cancers, and the associations are biologically plausible," Dr. Steven S. Coughlin, from the Centers for Disease Control and Prevention in Atlanta, and colleagues point out To investigate further, the researchers examined the relationship between diabetes and death from cancer in a group of 467,922 men and 588,321 women who were cancer-free when the study began in 1982. The findings are published in the American Journal of Epidemiology. After 16 years of follow-up, the authors uncovered a link between diabetes and death from colon and pancreatic cancers. In addition, in men, diabetes seemed to increase the death risk from liver and bladder cancers, whereas in women an association with death from breast cancer was seen. The researchers note that study had a number of limitations, but conclude that the findings "may help to clarify cancer risks for men and women with a history of diabetes mellitus." End.

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Cancer myths on way out-(Yahoo News-05/06/2004)

Some people still believe cancer is contagious or caused by a knock, but communities were vastly better informed about the deadly disease than 40 years ago. New research also has found cancer-screening rates have significantly improved, as have the number of people who believe lifestyle factors influence the development of cancer. Dr Owen Carter, whose research was published in today's Medical Journal of Australia, said confidence in cancer treatments also had increased but people were more realistic in their expectations of ultimate cure rates. Dr Carter, a research fellow at Curtin University of Technology's Centre for Behavioural Research in Cancer Control, said there was no doubt public education and awareness campaigns had had a "major and positive impact" on public perception, but there was still room for improvement.

The research compared responses to questions used in a 1964 survey of beliefs about cancer with those replicated in a 2001 telephone survey to track any changes. In 1964, 20 per cent of people thought cancer was contagious compared with 3 per cent in 2001, while the number of people who thought cancer was caused by a "knock" dropped from 25 per cent to 1 per cent. Conversely, more people now believe cancer is caused by lifestyle factors such as sun exposure (5 per cent in 1964, up to 16 per cent in 2001), diet (4 per cent to 26 per cent), worry and stress (3 per cent to 10 per cent) and smoking (22 per cent up to 43 per cent). The number of people willing to have a cancer check-up with no obvious symptoms has remained stable at about 85 per cent, but the number of people who have actually had a cancer check-up has jumped from 18 per cent to 77 per cent.

"The improved cancer-screening rate appears to reflect greater opportunities to participate in cancer screening, rather than great motivation to participate per se," Dr Carter said. More people now believe cancer was sometimes curable (82 per cent) than in 1964 (33 per cent), but fewer believe it is incurable (5 per cent) than 40 years ago (40 per cent). "The near-eradication of the belief that cancer is incurable perhaps reflects greater confidence in modern cancer treatments and that most participants had personal knowledge of someone successfully treated for cancer," Dr Carter said. The number of people who have personal knowledge of a cancer survivor rose slightly from 37 per cent in 1964 to 46 per cent in 2001. Most people get the majority of their information about cancer from parents and relatives now followed closely by television and newspapers. In 1964, newspapers were the leading source of information.

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Cancer gene MYC emerging as key research target-(Yahoo News-01/07/2004)

New technologies are shedding light on MYC's complex functions. First discovered twenty years ago, the cancer gene MYC is the most overexpressed oncogene in human cancers. But only in recent years have scientists begun to unravel MYC's complex workings in an effort to develop therapies that would block MYC's function in cancer. The promise of therapies targeting MYC appears especially great; MYC mutations are associated with a wide range of common cancer types, including breast, colon, ovarian and prostate cancers, and melanoma. Recent studies have determined that the MYC protein, known as a transcription factor, binds to about 15 percent of all genes. Scientists had long believed that when MYC binds to a target gene, it turns that gene on, or activates it. Surprisingly, new work by Steven B. McMahon, Ph.D., assistant professor at The Wistar Institute, and others demonstrates that MYC frequently binds to genes without activating them.

In an article for Nature Reviews Cancer published online today and in the July print issue, McMahon's research team offers a reanalysis of several previous studies of MYC's binding to target genes. The unexpected discovery that MYC binds to a large percentage of genes without activating them calls into question long-held assumptions about MYC's functioning and opens new directions for MYC research, McMahon says. "These previous studies looked at which genes are bound by MYC, and it turns out to be a great percentage of genes--one out of every six," McMahon says. "Our work has extended what these studies hinted at: contrary to what was believed, MYC doesn't always turn on the genes to which it binds. The implication is that just figuring out which genes bind to MYC will not be enough to tell us what pathways are being activated in cancer. There must be other factors that play a role in whether MYC activates a gene."

McMahon worked with colleague Louise C. Showe, Ph.D., associate professor at The Wistar Institute and scientific director of Wistar's genomics and microarray facility, on the reanalysis of the data from the previous MYC studies. Microarray technology enables scientists to study the activation patterns of thousands of genes at once instead of looking at single genes. Such analyses have become possible only in recent years, with the sequencing of the human genome and the development of powerful computers and computational methods for sorting through the data. The discovery that MYC binds to so many genes without necessarily activating them raises new questions for cancer researchers. Does MYC have other functions besides activating genes? Are there other unknown factors that play a role in whether MYC activates a gene?

"There are many other processes besides activation that MYC might be regulating," McMahon says. "It's also possible that there might be tissue-specific controls related to MYC binding." He notes that perhaps MYC binds to a given gene in all cell types but only activates that gene in a specific organ. Another question is whether this phenomenon of binding without activating may occur with other transcription factors besides MYC. "These kinds of studies and the technology enabling them are so new that many of these questions haven't yet been addressed," McMahon says. Already biotechnology companies are developing cancer drugs directed at MYC, but current efforts involve drugs that would block all MYC function. Understanding the specific targets of MYC and their involvement in cancer should ultimately allow scientists to create better drugs that would only block MYC function in cancerous cells, thus reducing toxicity, McMahon says.

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New Treatment Boosts Cancer Patient's Energy Drug Normally Prescribed For Hyperactivity-(EDT-01/07/2004)

New research shows that Ritalin -- a drug used to treat hyperactivity and attention deficit disorder -- could help cancer patients feel more energized. In hyperactive people, Ritalin works to stimulate the part of the brain that inhibits general activity. In a brain that is not hyperactive, however, Ritalin is being shown to increase brain function in a way that results in increased energy levels, NewsChannel 4 reported.

Dr. Eduardo Bruera, a researcher at the University of Texas M.D. Anderson Cancer Center, designed a study to see if Ritalin could increase a patient's energy level without causing side effects such as anxiety or insomnia. After one week of using Ritalin, more than 90 percent of Dr. Bruera's patients felt less fatigued and rested better at night. "I'm more rested even though I'm more energetic," Clauder said. "I'm not tired from doing things. I feel like I've had a good day at the end of the day. I feel like I accomplished something today." Doctors say about 90 percent of cancer patients feel fatigued, and it is difficult to treat patients for the symptoms. "I just wasn't myself anymore," said Sybil Clauder, a cancer patient. "I was just becoming something that lay on the bed all day and didn't do anything. My personality changed." For people without medical fatigue, Ritalin can cause insomnia, heart palpitations and arrhythmias.

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More Than 20 Million Die of Cancer Annually-(Yahoo News-25/06/2004)

Ghana Health Minister, Dr Kwaku Afriyie, has disclosed that over 20 million people worldwide die out of cancer each year. This figure, he said, included the young, old, poor and the rich. Dr Afriyie made this startling disclosure when he read a speech on behalf of the Vice President Alhaji Aliu Mahama at the launching of the cancer society of Ghana in Accra. He said, statistics from the World Health Organization (WHO) indicated that cancer was one of the most common causes of high morbidity and mortality rates, with more than 10 million new cases and 6 million deaths each year, worldwide. According to the minister, what was worrying the more was the fact that "half of all cancer cases occur in developing countries such as Ghana."

The minister further noted that the poor economic and social conditions in which Ghanaians lived, tended to compound matters and added that, to arrest the situation, the government initiated and implemented the Ghana Poverty Reduction Strategy (GPRS) aimed at reducing or totally eliminating poverty in the country. He further gave the assurance that the government was also enthusiastic to co-operate with the cancer society of Ghana as well as other NGOs in the war against cancer. "There is therefore the need for the development of a comprehensive national preventive and control programme as emphasized by WHO," he said. The minister, further suggested that the society as a matter of urgency, should draw proactive and pragmatic programmes with the aim of educating Ghanaians on cancer and also provide reliefs, consolation and comforting care through the provision of pain reliefs and psychosocial support saying, "There is therefore the need for the development of a comprehensive national preventive and control programme as emphasized by WHO."

In his address, Mr. Yaw Adu Boahen, a trustee of the society said the society was dedicated to the minimization of the incidence of cancer, commitment to helping everyone who faced cancer, through education, enhanced access to patient care, early detective and research commitment. He stated also that, they needed the collaborative effort of stakeholders to develop an accurate national research register and to implement appropriate educational access and palliative care strategies. He further outlined the objectives of the launching of the society as, signaling the people of Ghana on the existence of a cancer society, creating awareness, raising funds to support the society and alerting potential collaborators.

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Research on the potential oral delivery of a current intravenous cancer drug using polymeric nano-delivery systems technology-(Yahoo News-16/06/2004)

Labopharm today announced that it has entered into an agreement with Debiopharm S.A. to conduct research on the potential oral delivery of a current intravenous cancer drug using Labopharm's proprietary polymeric nano-delivery systems technology (also referred to as micelles technology). Labopharm's polymeric nano-delivery systems are composed of proprietary, low cost, block co-polymers developed specifically for effective delivery of water insoluble compounds and poorly bio-available compounds, including highly toxic compounds, such as cancer drugs. Suitable for oral and parenteral administration, these high capacity, biocompatible and biodegradable carriers are designed to maximize drug efficacy and to avoid many of the dose-limiting side effects of conventional approaches. With applications in oncology, immunology and a variety of other therapeutic arenas, polymeric nano-delivery systemsare expected to facilitate the delivery of both small molecules and emerging drug classes such as proteins, peptides and nucleic acids.

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Inflammatory Enzymes Linked to Cancer-(HealthDayNews-15/06/2004)

The first evidence that COX-2 enzymes, which are responsible for pain and inflammation, are also involved in causing DNA damage associated with cancer is outlined in a new University of Pennsylvania study. This finding provides new insight into how aspirin, along with diets rich in fruits, grains and vegetables, seem to reduce the risk of some cancers. The study also suggests that COX-2 inhibitor drugs, such as the anti-arthritis drugs rofecoxib (Vioxx) and celecoxib (Celebrex), may help prevent the DNA damage caused by COX-2 enzymes. The research was presented at the annual meeting of the American Society for Biochemistry and Molecular Biology / 8th International Union of Biochemistry and Molecular Biology Conference in Boston. The same presentation also included data supporting earlier research that large quantities of vitamin C can increase DNA damage.

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Osaka Pref. faces highest risk of cancer due to polluted air-(The Daily Yomiuri-18/06/2004)

Residents in major urban areas and surrounding regions are more likely to develop cancer caused by chemical substances in the air, recent research has shown. According to research conducted by Michi Matsumoto, chief researcher at the National Institute for Environmental Studies, and others, Osaka Prefecture residents are more than five times likelier to develop cancer than Tottori Prefecture residents. The research measured the density of five substances that are discharged into the air and are proven to be carcinogenic, including benzene and formaldehyde. The research is the first to measure the cancer risk by prefecture. The results will be presented at an open symposium given by the institute.

According to the research, the prefecture with the highest cancer risk from polluted air is Osaka, followed by Tochigi, Kagawa, Saitama and Kanagawa prefectures. Meanwhile, the prefecture with the lowest risk is Tottori, followed by Ishikawa, Toyama, Shimane and Miyazaki prefectures. The data do not include Akita, Yamanashi, Nagano and Fukui prefectures, which have no measured value of formaldehyde. The calculation indicates that 9.2 Osaka Prefecture residents and 1.6 Tottori Prefecture residents out of every 100,000 residents develop cancer by regular contact with the polluted air. However, the cancer risk from inhaling the air is only about one-thousandth of the cancer risk of smoking tobacco every day.

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Pfizer Buys Cancer Drug Rights from Sanofi NEW YORK (Reuters-18/06/2004)

Pfizer Inc. said it agreed to acquire the rights it doesn't already own to a colorectal cancer drug from Sanofi-Synthelabo for $620 million, to strengthen its oncology business. The acquisition will give Pfizer a stronger presence in the European market, where it currently has no flagship oncology drug. Pfizer only markets the product in North America, Latin America, Australia and New Zealand. Aventis sells the drug everywhere else except Japan. Sanofi-Synthelabo, which is acquiring Aventis for $61.63 billion, is required by anti-trust authorities to divest assets that would give it a monopoly.Camptosar, known as Campto in Europe, and Sanofi-Synthelabo's Eloxatin, are the two leading metastatic colorectal cancer chemotherapies. "The addition of Campto strengthens our oncology presence in the European market and it provides us with an opportunity to bring together our clinical development programs," said Paul Fitzhenry, a Pfizer spokesman.

Pfizer is testing the drug's effectiveness in other cancers, particularly lung cancer. Despite being the world's biggest drug-maker, Pfizer has a tiny presence in the field of oncology. Of its $45 billion in sales last year, roughly $1 billion came from cancer drugs, and of the 20 products it expects to have submitted for marketing approval in the five years ending 2006, just two are for cancer. Bill Slichenmyer, Pfizer's vice president of oncology drug development, said the company is determined to change that. Oncology now accounts for 12 percent of the company's research budget, second only to the cardiovascular research, he said. "We feel we have the critical mass now to expect more successes ahead," he said. "We hope that in a few years time it will become evident that Pfizer will become a leader in oncology." Slichenmyer said the company has 16 different cancer drugs in testing today, of which two are in late stage development, six are in mid-stage and eight are in early-stage.

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Age, race and sex disparity found in cancer research trial participation-(Yahoo News-08/06/2004)

Although people age 65 and older account for 62 percent of patients with lung, colon, breast or prostate cancer, they make up only 32 percent of cancer research participants, Yale researchers report in the June 9 Journal of the American Medical Association. "We found that cancer research participation varied significantly across sex and racial/ethnic groups as well as age," said principal investigator Cary Gross, M.D., assistant professor of internal/general medicine at Yale School of Medicine. "Enrollment in cancer trials is low for all patient groups, but the elderly, racial and ethnic minorities, and women were less likely to enroll in cooperative group cancer trials than were whites, men and younger patients. Overall, less than two percent of adult patients with cancer are enrolling in research studies."

Gross and co-authors analyzed data on participants in the therapeutic non-surgical National Cancer Institute Clinical Trial Cooperative Group. This included breast, colorectal, lung and prostate cancer clinical trials from 2000 through 2002. In a separate analysis, the ethnic distribution of patients enrolled in 2000 through 2002 was compared with those enrolled in 1996 through 1998. Gross said that while the total number of cancer patients enrolled in research studies increased by almost 50 percent between 1996 and 2002, the proportion of trial participants who were non-white declined during this time period. The team found that while blacks had significantly lower enrollment rates in breast, lung and colorectal cancer trials compared with whites, the representation of blacks and whites in prostate cancer trials was comparable.

"This shows that equitable representation between races is possible, and investigators should assess how the prostate cancer researchers were so good at recruiting black patients," said Gross. The study also demonstrates that elderly patients, both minorities and whites, were strikingly underrepresented compared with their non-elderly counterparts. "This low participation rate has been remarkably consistent over the past decade," said Gross. "These findings are of concern, given the substantial cancer burden borne by minorities and the elderly," Gross added. "It is apparent that other policies and initiatives will be required to ensure broad access to trials and broad applicability of their results."

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Patients living longer as progress is made in fight against cancer-(ET-03/06/2004)

Significant strides are being made in the fight against cancer, and patients are living longer, as Americans' risk of contracting and dying from cancer declines, a new report revealed. Death rates have dropped for 11 of the 15 leading cancers among men, and for eight of the top 15 in women, the American Cancer Society reported, citing the "Annual Report to the Nation on the Status of Cancer, 1975-2001." Overall cancer rates fell 0.5 percent per year between 1991 and 2001, and death rates from all forms of cancer declined 1.1 percent a year between 1993 and 2001. For men, the rate of contracting cancer of the lung, colon, oral cavity, stomach, pancreas and larynx has decreased, along with the incidence of leukemia, while the rate of contracting melanoma and cancers of the prostate, kidney and esophagus has increased. Among women, the incidence of lung cancer is down for the first time, according to the American Cancer Society. The incidence of colon, cervical, pancreatic, ovarian and oral cavity cancer also decreased in women, while melanoma and breast, thyroid, bladder and kidney cancer were on the rise.

"Cancer is a devastating disease that impacts so many people. But the good news is there is hope, and these data show we are winning the battle as people with cancer are living longer and more healthier lives than ever before," said Julie Gerberding, director of the US Centers for Disease Control and Prevention. Nearly 25,000 oncologists from around the world are expected in New Orleans, Louisiana, on Saturday for the 40th conference of the American Society of Clinical Oncology (ASCO), and the findings of the report are to be a leading topic of discussion.

A total of 3,700 studies will be presented at the ASCO meeting, highlighting topics from "immediate implications for prostate cancer patients" to "important research on agents for reducing the risk of breast and colorectal cancer," organizers said. Studies on the effectiveness of using certain genetic markers to predict how a patient will respond to treatment will also be presented, along with progress in targeted therapy, which allows cancerous cells to be destroyed while sparing healthy cells.

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Smuggling cancer drugs into the body-(Yahoo News-02/06/2004)

Scientists have taken a big step forward in their effort to find a new weapon against cancer. Researchers have been carrying out tests on a potential new drug that targets cancer tumours without harming healthy tissue. However, they have struggled to deliver the drug directly to tumours because the immune system attacks it before it can get to work. Now researchers at Cancer Research UK believe they may have found a way around the problem. They have managed to disguise key elements of the drug and smuggle it into the body undetected.

The drug, called monoclonal antibodies, is delivered into the body using a technique called Antibody Directed Enzyme Pro-Drug Therapy or ADEPT. This technique involves injecting patients with an enzyme or protein that attaches itself to cancer cells. Patients are then injected with monoclonal antibodies. These drugs are only activated when they encounter the protein. They lock onto the protein and cause the body's own immune system to start attacking the cancer cells too. They can also cause the cancer cells to destroy themselves. Trials of these drugs have so far had limited success because the immune system sees it as a threat. The scientists hope their discovery will boost efforts to develop these drugs as a possible new treatment.

"Minimising the immune response...will increase the potential of many forms of ADEPT for clinical use," said lead researcher Dr Astrid Mayer, who is based at the Royal Free and University College Medical School. Professor Robert Souhami of Cancer Research UK welcomed the findings. "This study has identified a relatively simple method of reducing the body's reaction against this enzyme," he said. "Finding ways of disguising the molecular features of certain cancer therapies could make them safer and more effective." The study is published in the British Journal of Cancer.

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Do We Need Cancer Checks At 80?-(CBS News-17/05/2004)

Does an 80-year-old really need a Pap smear? Do mammograms in the 70s find dangerous breast cancer or tumors that are too slow-growing to threaten women's last years? The question of when you're old enough to quit routine cancer checks is a tough one. And new research suggests it's one that many doctors and seniors avoid tackling: Tens of thousands of elderly women in California alone are getting mammograms and Paps even though their overall health is too poor to benefit. Are doctors scared to tell such patients to stop? "I think so," says Dr. Louise Walter of the University of California, San Francisco, who led the study in that state. "You don't want anyone to ever think you're giving up on them." But it's an important decision, because at some point the benefits of cancer screening can be outweighed by the harms - unnecessary treatment, or additional testing and anxiety from false alarms. "In older people, (screening) is very much a choice," Walter says. "These discussions need to be had."

Most cancer groups are pretty specific on when Americans should start getting screened: Pap smears to detect cervical cancer should start within three years of sexual activity and no later than age 21. Mammograms to spot breast cancer start at 40. Colon cancer tests start at 50. PSA or "prostate specific antigen" tests for prostate cancer usually are offered then, too. Screening is encouraged earlier if cancer runs in the family or people have other risk factors. When to quit is murkier. Guidelines now recommend ending Paps at age 65 or 70 if the woman has no history or recent signs of cervical cancer. It's typically a slow grower that's almost always caused by a sexually transmitted virus. The other malignancies have no definitive cutoffs. But specialists are rewriting guidelines to reflect that seniors should continue getting routine cancer screening as long as their life expectancy makes it likely they'll benefit - about another five years for mammograms, 10 years for men's PSAs. (No word yet on colorectal screening.)

Most screening is important for vibrant seniors, says Dr. Robert Smith of the American Cancer Society. After all, a 70-year-old without serious medical problems has a life expectancy of 15 more years. "If she could live to be 85, we don't want her to die of breast cancer at 79," he says. Yet life expectancy is difficult to predict, and to discuss. "Primary-care physicians tell us of sitting there with a person in heart failure who suddenly announces that isn't it time for their mammogram," Smith says. "It's very awkward for them to say that wouldn't be a good use for scarce resources."

The California research, published this month in the Annals of Internal Medicine, highlights the confusion. It estimates that 97,000 healthy California women ages 70 to 84 are skipping mammograms - although they could benefit - while 81,000 unhealthy women 80 and older still get them. Walter derived the estimates by analyzing health survey data from 4,700 elderly women. She found 72 percent of the 80- to 84-year-olds surveyed reported a recent Pap smear, despite guidelines that suggest most were unnecessary. Some women even reported recent Paps though earlier hysterectomies for noncancerous reasons had left them with no cervix and thus no need for the test. Walter estimated that number could reach 200,000 Californians. Medicare pays for elder cancer screening, and some people are reluctant to quit. They think, "'This is something I do when I'm healthy. If I don't do it, it means I'm not healthy,"' Walter says.

While risk of cancer increases with age, heart disease and other age-prone killers increasingly take a bigger toll. Breast cancer causes 12 percent of deaths among 50-year-old women, but just 3 percent of deaths among 75-year-olds, Dr. Gilbert Welch with the Veterans Affairs Medical Center in Vermont notes in an editorial accompanying Walter's research. Yet it's hard for many people to understand that cancer can grow slowly enough that an elderly person will die of another disease before the tumor ever becomes threatening. Walter urges seniors to have a candid talk with their doctor. Ask: Am I a good candidate to continue screening? What happens if suspicious signs are found? Will I need a biopsy or other testing? What does treatment entail? And remember, it's reasonable to shun aggressive treatment at 80 that you might have chosen at 50, says the cancer society's Smith -- so consider all your options.

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Drug trials put focus on older people with cancer-(Yahoo News-09/05/2004)

There aren't many people who, after being told they have advanced, terminal cancer, have reason to feel lucky. Armon Johannsen is one of those few. But that's not the only thing that sets the Fort Collins resident apart. For one thing, he's alive. Two years ago when doctors found a tumor in his lungs and it turned out to be melanoma, "they gave me just a few months," he said. Johannsen also is a 69-year-old cancer patient who is part of a clinical trial testing a new chemotherapy drug. And that makes him remarkable.

Cancer is, most of the time, a disease of older people. Decade after decade, the National Cancer Institute's statistics tell the same story: The older you get, the more likely you are to get cancer and the more likely you are to die of cancer. At the same time, the older you get, the less likely you are to be part of a clinical trial testing new and in some cases breakthrough treatments.In a study published last year, researchers from the National Cancer Institute analyzed nearly 500 cancer-treatment trials. They found that while 61 percent of all new cancer cases occur in people age 65 or older, people in that age group made up only 32 percent of clinical trial participants. But that is starting to change.

An infusion of grant money; simultaneous nudges from the National Institute on Aging, the National Cancer Institute and a private foundation; and publication of a handful of studies on the issue and its repercussions are at the vanguard of a movement to include the elderly in tests of new treatments. Last year, the National Institutes of Health, along with the nonprofit Friends of Cancer Research and five drugmakers, gave out nearly $6 million in grants to six institutions across the country - including the University of Colorado Cancer Center - to study ways to make tests of potential cancer treatments more inclusive. This year, the American Society of Clinical Oncology gave CU's cancer center more money, this time to recruit older people into clinical trials. The goal of the first study "is to identify barriers and then to do interventions and make it more feasible to have geriatric patients in clinical trials," said Dr. Michele Basche, who is leading the CU research.

Accomplishing that is important, and not just for people such as Johannsen desperately searching for a way to stay alive. It's important for the millions of baby boomers staring down old age who will demand doctors' latest and best. It's important, too, for the oncologists who treat people such as Johannsen now but can't be sure how someone in their 60s - or 70s or 80s - will tolerate toxic chemotherapy drugs that can debilitate patients in their 20s and 30s. "The way elderly patients respond to treatment is different," said Dr. Tim Byers, an oncologist and epidemiologist at the University of Colorado. That is true for many reasons, doctors say. "As people age, there are bone-marrow changes, renal- function changes, and all that can affect treatment," Basche said. "And there are some malignancies in which the biology is actually different," she said.

One such cancer is a type of leukemia, Basche said. And in the case of non- Hodgkin's lymphoma, a malignant growth of blood cells in the lymph system, older people are significantly less likely to be alive five years after their diagnosis, she said. Basche said that is partly because older people can't tolerate treatment as well. "But even if they tolerate it, it doesn't work as well" in older people, she said.

The problem for doctors is that in many cases, elderly patients don't walk into their offices with just cancer. Their disease comes in a package that may include other common plagues of age, such as diabetes, heart disease, kidney problems, obesity. And patients may be on medications to lower cholesterol, thin their blood or unclog their arteries. All those conditions and medications potentially impact and interact with anti-cancer drugs. Trouble is, doctors have little evidence of what those impacts and interactions will be. The study may be in its infancy, but Basche's experience has given her a few clues about what those barriers might be. "I had a patient who was 82, with metastatic colon cancer," Basche said. "But she had to care for her husband who had dementia. She had a lot of questions (about chemotherapy treatment) - 'How will I tolerate this? Can I still care for my husband? Will it really prolong my life?' But without the data, the answers we can give her are limited."

People of all ages can be nervous about serving as "guinea pigs," taking drugs not yet approved for widespread use. That fear can be especially pronounced among older people, Basche said. But many of the barriers are erected by medical institutions. "Since we're testing new treatments, we tend to be conservative," Byers said. "So we set up rules saying people can't come into clinical trials if they have other complications. "The trouble is that at the end of the day, or the end of the decade, we have a new treatment but we don't know what the risks are to people with co-morbid conditions." Still, one of the biggest barriers - the refusal of Medicare to cover the costs of care given to people enrolled in clinical trials - was removed in 2000. That same year, a researcher from New York University told the American Society of Clinical Oncology that she had found that doctors invited 51 percent of patients under 65 to consider trying an experimental drug but asked only 33 percent of patients over 65 if they wanted to participate in a clinical trial.

Basche speculates that some doctors may worry that elderly patients aren't well enough to cope with the side effects of an experimental drug. That is one barrier Johannsen didn't face, however. "My oncologist up here encouraged me to try a Phase 1 trial," he said. After checking out his options - which were few - Johannsen took the advice. "With Stage 4 melanomas, there is nothing out there that gives you a good chance," he said. "And the traditional things they do have side effects so severe and results so minimal that I just decided, 'What the heck?' I'd take my chances with a trial." That's how Johannsen wound up driving to CU, at first every day for a few weeks, and now every few weeks, for injections of a drug that so far bears the unflashy name of PI88. In 2001, CU became the first U.S. site to conduct trials of the drug, according to the Australian company that makes it. Johannsen is doing so well on the drug - which basically tries to starve tumors by cutting off the blood supply to them - that now when he drives to CU, he picks up a supply of the drug and injects it himself for four days every other week. His tumors haven't gone away, but they haven't grown, either. He'll take that, Johannsen said. And he credits the experimental drug with giving him the past two years, which doctors had said cancer wouldn't let him have.

That kind of decision should always be left up to the patient, Basche said. And it's never OK to assume that because someone is older, that patient isn't prepared to fight the disease. "Older patients wish just as much as younger patients to live long enough to see a grandchild's graduation or a new baby born into the family," Basche said. "It's not appropriate to assume that because someone is 82 that they're ready to die."

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Cancer treatments will be tailored to patients' genes-(Yahoo News-27/04/2004)

Doctors have taken the first steps towards identifying genetic differences between cancer patients so that treatments can be tailored towards a person's genetic make-up. The aim is to separate cancer patients into those who will respond to one particular form of therapy and those who will get better with a different type of treatment. Scientists believe that the personalised treatment of cancer could improve survival rates because the effective- ness of existing drugs and chemotherapy can vary depending on the patient. The latest research has been carried out by a team led by Mike West, a British-born professor of medical statistics at Duke University in Durham, North Carolina, who analysed the genes of 158 women with breast cancer.

The researchers used "gene chip" technology to investigate simultaneously the activity levels of more than 12,500 genes in breast-tumour biopsies taken from the women and banked between 1991 and 2001. Using statistical analysis, the scientists discovered patterns of gene activity in the tumours and used them to predict a patient's prognosis, such as the recurrence of the cancer after two or four years of treatment. Results of the study, published in the online issue of the Proceedings of the National Academy of Sciences, showed that the researchers were able to identify high-risk cancer patients with an accuracy of about 80 per cent. Mr West said the new genetic information could be used alongside more conventional clinical data to predict more accurately whether, for example, a woman would respond to aggressive therapies or whether she would be better suited to more benign treatment. Mr West said: "It is primarily traditional clinical information alone that aids in understanding a patient's risk profile. "The resulting predictions typically group patients into broad categories. Access to detailed genomic information provides the opportunity to move far beyond this towards customised risk predictions and prognoses more widely for the individual patient. This study is the validation of the concept that this kind of molecular genetics information will have an impact on clinical decision making."

The gene chip used in the study was manufactured by the Californian company Affymetrix which has specialised in making test kits that can simultaneously measure the activity levels of thousands of genes. Scientists believe gene chips can help determine genetic differences between patients that could determine the way the disease will progress. Richard Sullivan, the head of clinical programmes at the charity Cancer Research UK, said analysing the genetic make-up of cancer patients in order to tailor treatment towards the individual was the "Holy Grail" of cancer therapy. Dr Sullivan said: "Adjuvant chemotherapy, for instance, only benefits two out of ten women with breast cancer and we don't know who those people are. "We have a real problem with over treatment. The ideal situation is to spot the women who are really going to benefit, and those who are not. "The other issue is toxicity because some people react extremely badly to drugs."

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Blood screen may help cancer patients thwart radiation side effects, say Stanford researchers-(Yahoo News-19/04/2004)

Radiation therapy is a powerful tool for treating cancer, but for 5 percent of patients that lifesaving treatment comes with serious side effects. Screening blood for the activity level of 24 genes may identify those patients most likely to react badly to radiation, say Stanford University School of Medicine researchers. With this tool, doctors may soon be able to tailor-make treatments for individual patients. "We've been treating cancer patients as if one treatment fits all," said Gilbert Chu, MD, PhD, professor of medicine and of biochemistry who led the study. "Cancer patients need to be treated for their particular cancer and their own bodies."

Some factors are a tip-off that a patient may have an unusually severe reaction to radiation. Patients who have autoimmune diseases such as diabetes or lupus, or who have certain rare genetic diseases need to be monitored carefully or avoid radiation altogether. Even beyond these obvious signs, some patients suffer disfiguring, disabling or extremely painful effects. These may include wounds that don't heal, skin burns so severe they require plastic surgery, or brain damage. Past attempts to identify these patients by screening the cancer cells themselves have failed, according to Chu. In his study, published in this week's online edition of the Proceedings of the National Academy of Sciences, Chu and colleagues describe 24 genes that can be used to single out these patients for alternate therapies or lower radiation doses. Chu said screening blood rather than cancer cells means the test would be more accessible to patients. "To be most useful it had to be done on peripheral blood and with a small number of genes," he said.

Chu, whose research revolves around how cells repair damaged DNA, thought that patients who respond poorly to radiation might have cells that don't properly recognize or repair radiation-induced DNA damage. These cells may turn on different genes, or the same genes at different levels, compared with normal cells exposed to radiation. A group of graduate students and medical students consisting of Kerri Rieger, Wan-Jen Hong, Virginia Goss Tusher and Jean Tang tested this idea in blood samples taken from 57 cancer patients who had recently received radiation treatment. Of these, 14 patients had unusually severe radiation toxicity. The students used a gene microarray, which provides a snapshot of gene activity, to analyze which genes were active in blood cells. In the initial analysis, Chu said the group couldn't identify genes that were consistently different between patients who did and didn't suffer serious side effects. He worked with Robert Tibshirani, PhD, professor of health research and policy, to develop a new statistical method of analyzing the microarray data.

With this improved analysis, the group found 24 genes that behaved differently in patients who suffered radiation toxicity. When Chu and his colleagues tested the patients' blood samples for these 24 genes, they identified nine of the 14 people with severe reactions. Of the remaining five patients, two were later found to have been treated with new approaches that carried high risks for toxicity. That left only three of 14 patients who the test failed to identify. Most important, the test did not mistakenly pinpoint any of the other patients. Knowing which patients may have severe radiation toxicity could make treatment decisions easier. For cancers of the breast or prostate, Chu said surgical options can be as effective as radiation. "If you knew one of the options carried a big risk, that might alter your decision," he said.

For other cancer patients, radiation may be the best treatment. However, Chu added that patients at risk for high toxicity may also have cancers that die in response to much lower radiation doses. In such cases, radiation - though at greatly reduced doses - may still be an option. Those who don't have severe radiation toxicity may also benefit from this study. "If you eliminate those patients with toxicity you may be willing to use higher doses for the remaining patients," Chu said. He said doses are set by what an average person can handle. If patients are treated individually rather than as averages, many could receive higher, more effective doses. Chu said that before personalized treatment becomes possible, researchers must validate the 24-gene test on a larger number of samples. A biotech company must also commercialize the screen and make it available to medical labs.

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Center Uses Laser Method to See Cancer-(Yahoo News-19/04/2004)

Xerox Corporation's Palo Alto Research Center, which developed some of the standard techniques now used in personal computing, is moving into biotechnology. The research center, known as PARC, quietly formed a partnership two years ago with the Scripps Research Institute in San Diego. Now, the Scripps-PARC Institute for Advanced Biomedical Sciences, as the partnership is known, is announcing its first potential product: a system based on laser printer technology to detect cancer cells. PARC is not the first high-technology organization to seek new, and possibly greener, pastures in the life sciences, which increasingly rely on computers and sophisticated electronic instruments. Agilent Technologies, Corning and Motorola, for instance, made forays into the market for DNA chips, which measure gene activity and can be made using semiconductor or ink jet printing technology.

Richard H. Bruce, who runs biomedical research at PARC, said that because his organization did not have people trained in life sciences, it relied on Scripps, a well-known medical research center in San Diego, to define the problems to which PARC's technology could be applied. "We asked them to tell us 10 problems that if we solved would have a big impact," said Dr. Bruce, a physicist who is in charge of PARC's computer science laboratory. One problem was to search the bloodstream for cells that slough off tumors. Detecting such cells could allow doctors to detect cancer early or to monitor the success of therapy. But such cells exist, Dr. Bruce said, in concentrations of one in a million or one in 10 million blood cells, meaning that 50 million or more cells in the blood might have to be checked to find them. The technique developed by PARC and Scripps involves tagging cancer cells with a fluorescent marker and then scanning the blood cells with a laser looking for fluorescence. "It's basically like scanning paper," Dr. Bruce said. He said it could narrow 50 million cells to 500 possible cancer cells in minutes. Existing techniques, he said, can take 30 hours.

Dr. Bruce said that if further testing proves the device works as expected, PARC would try to commercialize the device, either by licensing it to a company or by starting a company.

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Breathalyser could detect cancer-(Yahoo News-05/04/2004)

The cancer "breathalyser" works using technology originally designed for oil prospecting. It uses lasers to detect tiny traces of ethane in the breath, and is so sensitive it can spot concentrations of less than one part per billion. The University of Glasgow project aims to detect lung cancer from ethane released by cells breaking down. The project's Dr Kenneth Skeldon said: "Early detection and monitoring of cancer and other serious diseases hugely improves the effectiveness of treatment and the possibility of cure.

"People can produce a higher trace of ethane in their breath when cancer strikes. It turns out that the amounts involved are similar to those given off by an oil reservoir. "Our technology was first developed with that area in mind, but now we are sniffing out human ethane using advanced laser technology." The research is being conducted jointly with the company BOC, which is providing the pure gases and ultra-clean pumps needed to make the device work.

An estimated 30,000 people die from lung cancer each year in the UK, and only about 5% of sufferers survive five years after diagnosis. The disease can lurk in the body for up to 20 years before any symptoms appear. By the time it is detected it is often too late. The new device, dubbed the "laser nose" by experts working on the prototype, could potentially help doctors detect signs of lung cancer earlier. Nick Ward, business manager for BOC Scientific, said: "Patients could have an immediate answer on their condition, ending the agonising wait for normal cancer test results."

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Discoveries on genomic instability have moved cancer prevention in new directions-(EurekAlert-25/03/2004)

Frederick W. Alt, a Howard Hughes Medical Institute investigator at the Children's Hospital Boston Department of Molecular Medicine, has received the Clowes Memorial Award from the American Association for Cancer Research, acknowledging his three decades of seminal discoveries in genomic instability and cancer. The Clowes is the oldest award given by the AACR, and recognizes outstanding recent accomplishments in basic cancer research. The award will be presented at the AACR's 95th Annual Meeting in Orlando, Fla. (March 27-31, 2004). This month Alt, who holds a doctorate in Biological Sciences, also received the prestigious Scientific Leadership Award in Immunology from the Irvington Institute for Immunological Research in New York City. Alt was the first to elucidate a molecular mechanism for genomic instability (an increased tendency to develop gene mutations) involved in promoting cancer.

The human genome is at constant risk for mutations due to environmental insults, errors in gene replication, and other factors that can cause chromosomes to break and bits of DNA to be lost, duplicated, or reshuffled to the wrong chromosomes (translocated). Cells have repair mechanisms that constantly fix this damage, but when the repair process breaks down, the genome becomes unstable and cancers are more likely to develop. Alt's wide-ranging research has important implications for cancer prevention and has sparked much additional research by other scientists. His work has touched on many aspects of genomic instability and cancer.

Several key advancements specifically cited by the AACR are detailed below, followed by a description of Alt's more recent work. Alt's early work, as a student with Robert Schimke in the 1970s, led to the discovery of a major form of genomic instability known as gene amplification, or creation of many duplicate copies of a gene, sometimes even numbering in the thousands. Studying how cancers become resistant to the chemotherapy drug methotrexate, Alt studied how cancer cells churn out high levels of an enzyme that enables the resistance. He showed that gene amplification endows these cells with many extra copies of the gene encoding this enzyme. "At the time, people believed the mammalian genome was inviolate and didn't change at all," recalls Alt, who is also the Charles A. Janeway Professor of Pediatrics at Children's and a professor of Genetics at Harvard Medical School. "This discovery showed that cancer cells, at least, could change their genome drastically, and was the first clear-cut molecular demonstration of genomic instability in cancer."

The gene amplification work led Alt to co-discover a specific cancer-causing gene, or oncogene, known as N-myc. He found that N-myc is frequently amplified in neuroblastoma, a childhood brain cancer, making the cancer especially aggressive. "N-myc opened up oncogene amplification as important in cancer prognosis and in mechanisms of cancer progression," he notes. Oncogene amplification has since been found to be fundamental in many advanced-stage cancers, but Alt's N-myc discovery in the early 80s provided one of the first systematic associations with a particular tumor.

During the 1980s, Alt also turned his attention to immunology studies, examining how the immune system can recognize and defend against an almost infinite variety of attackers. Serendipitously, this work also led to key discoveries about genomic instability. The immune cells known as T lymphocytes have receptors that can recognize far more foreign invaders than the genome could possibly anticipate and encode for. The same is true of B lymphocytes, which can make a seemingly limitless variety of antibodies. The genes for these receptors and antibodies come in segments known as Vs, Ds, and Js. In collaboration with Nobel Prize Winner David Baltimore (now president of the California Institute of Technology), Alt helped elucidate how these gene segments are cut and pasted into millions and even billions of combinations through a process known as VDJ recombination. Baltimore subsequently discovered the proteins that do the cutting, known as recombination activating gene (RAG) proteins, but Alt speculated that some other mechanism was pasting the Vs, Ds, and Js back together. Knowing that cells have a variety of tools for general gene repair, he theorized that those same tools recombine V, D, and J gene segments for the immune system.

In the early 1990's his lab studied numerous different kinds of hamster ovary cells that were known to be defective in gene repair, and added RAG proteins to cut apart the V, D, and J segments. They then investigated which cell types could and couldn't reassemble the segments. Three of the cell types couldn't complete the VDJ recombination, and further studies of these cells led to the discovery of major components of the non-homologous DNA end-joining pathway. This pathway not only joins the severed V, D, and J segments, but also has a key role in maintaining genomic stability by mending double-strand breaks in DNA molecules. Alt and his collaborators immediately identified three proteins involved in this pathway, and later elucidated roles for two more; a total of six end-joining proteins are known today. Alt's team found that mice deficient in these proteins, in combination with certain other mutations, are dramatically susceptible to cancers of the immune system and other cancers. Mechanisms of oncogene amplification and translocation Alt's lab also has demonstrated that when a cell is deficient in both end-joining proteins and a protein known as p53, gene amplification, translocations, and tumor formation are greatly enhanced.

Normally, p53 sets up a "checkpoint" that detects cells with unrepaired chromosomal breaks, and either kills them outright or prevents them from growing and dividing. In its absence, genomically unstable cells remain in circulation and accumulate more mutations, becoming increasingly malignant. (The p53 protein is known to be mutated in almost half of human cancers, including breast, colon, lung, and prostate cancer.) When cells lacking both p53 and having defective end-joining proteins fail to repair chromosome breaks, the breaks are replicated along with the chromosome during cell division. The broken ends join to broken ends on other chromosomes, causing cancer-initiating translocations. As chromosomes keep breaking, fusing their broken ends, and replicating, gene amplification results as extra copies accumulate.

Alt's more recent work is exploring further mechanisms of genomic stability in cancer. One mechanism involves H2AX, a structural protein that helps ensure that double-strand DNA breaks are properly repaired by the end-joining proteins. When p53 is also absent, loss of even a single copy of the H2AX gene can lead to translocations. "If you eliminate H2AX and P53 in mice, they get all sorts of cancers - lymphomas, solid tumors, you name it," Alt says. Interestingly, simply reducing H2AX activity is enough to cause genomic instability. "You can't just think that a tumor suppressor gene has to be completely mutated or gone to contribute to cancer," he says. "We need to think in a new way about tumor suppressive genes, particularly those involved in genomic stability." H2AX is a prime candidate for further study, because it maps to a region of human chromosome 11 that is altered in a large percentage of human cancers. A second mechanism, again drawing on Alt's work in immunology, is class switch recombination. This gene-reshuffling tool is used by the immune system to instruct an antibody where to go in the body and what strategy to use in fighting a pathogen. As with VDJ recombination, genes are cut and pasted, generating different classes of antibodies (IgM, IgG, IgE, etc.). Again as with VDJ recombination, Alt believes that errors in the "pasting" part of the process may lead to translocations and oncogene (cancer gene) activation, a phenomenon already seen in many human B-cell lymphomas. H2AX may play a protective role here as well, Alt believes, by ensuring that cut ends of genes are properly joined.

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Mushrooms Play a Role in Cancer Research-(Yahoo News 23/03/2004)

The statistics are startling. One in three women get cancer. Half of all men do. With odds like that, it is understandable why millions, if not billions, of dollars are spent every year in this country on cancer research. And that research involves everything from the largest pharmaceutical firms to state of the art medical complexes and even one man in the Ozarks and his crop of mushrooms. His name is Tim Hite and he's lost both friends and family to the disease. For that reason, he's dedicated his life to looking into alternative forms of medicine. Hite lives in Ozark, Missouri. But he spends most of his time in his greenhouse. That's where Hite grows 25 varieties of mushrooms. "Most of the mushrooms we're growing in here are drying. We're blending them into teas," says Hite.Hite grows the precious fungus at an amazing rate. He is able to grow 2,000 pounds of mushrooms in a month. "What we're involved in is growing gourmet mushrooms. Oyster, European variety," Hite notes. While the mushrooms may be gourmet, Hite is not on a mission to feed the world. He's more interested in curing it of cancer.

"They've proven in a laboratory environment that this mushroom causes neurons to regrow so they are doing medical research on it for disease and disorders. We've developed some new techniques where we can actually quantify and qualify the amount of active ingredients in mushrooms for fighting cancers and different diseases. Hite says he has lost relatives and friends to cancer, which motivates him to keep growing the fungus. Hite says he has always been interested in alternative forms of medicine and it's his belief that that mushrooms may be able to provide some immediate relief to people sufferingfrom cancer. "One thing about traditional cancer treatment is it tears the body down. Chemotherapy is devastating to the body. These help rebuild the system so there are less adverse affect from radiation."

Hite grows the mushrooms and puts them into medicinal teas for cancer patients at both Cox and St. John's hospitals. And he's excited because he just got a grant from the state of Missourito continue his medical research. The grant allows people who have innovative ideas to give them funding to help demonstrate whether the idea will work. Under the grant program, farmers throughout the state can receive up to $3,000 to try innovative projects. Hite says he'll use that money to buy growing tanks and an irrigation system. Beyond the cancer research, Hite is using the mushrooms to reduce yard waste. Mushrooms are an excellent decomposer of forest debris and he plans to work with the city of Springfield about putting the mushrooms into the recycling centers.

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Hope For Infertile Women After Cancer Therapy-(PTI-19/03/2004)

Cancer patients of child bearing age, who may otherwise have difficulty conceiving a child after chemotherapy, radiotherapy and radical surgery can now look to a promising research for hope. US researchers report promising findings of a technique which could potentially help women to regain fertility after early menopause due to cancer therapy. Results of the technique on a 30-year-old woman are reported in a fast-track study published in the current issue of Lancet. One of the ways to possibly preserve fertility before these treatments is to freeze (cryopreserve) ovarian tissue for later transplantation. Kutluk Oktay and colleagues from the Center for Reproductive Medicine and Infertility (CRMI) of NewYork-Presbyterian Hospital/Weill Cornell Medical Center, USA, cryopreserved ovarian tissue from a 30-year-old woman with breast cancer before chemotherapy-induced menopause. This tissue was transplanted beneath the skin of her abdomen six years later. The patient's ovarian function returned after three months, and in-vitro fertilisation resulted in the development of a four-cell embryo which was implanted into the woman, although she did not become pregnant. "This research represents a potentially significant reproductive advancement in two respects: first, women can preserve their fertility by freezing their ovarian tissue, and second, pregnancy may be possible even after the tissue remains frozen for a long time," says Dr Oktay.

However, Johan Smitz from the Centre For Reproductive Medicine, University Hospital of the Vrije Universiteit Brussels, cautions that cryopreservation and transplantation techniques for certain cancer cases are not without risk. "In light of the current uncertainty about the effectiveness and safety of ovarian cryostorage and grafting, the whole procedure should still be presented as experimental to patients. Only a small part of the ovarian graft can be screened with sensitive techniques for the detection of hosted cancer cells". "For some cancers: those that colonise the ovary or that can metastasize into ovary, it will be always difficult to completely exclude the presence of such cells in the graft. " "To provide an evidence-based approach in future practice, a multicentre trial could be proposed in which girls or young women at intermediate risk of sterility would be randomised between storage of gonadal tissue or non-intervention." Such a prospective study would show which of the two options gives the best chances for obtaining a normal child. Whole-ovary freezing that allows vascular reanastomosis and more in-vitro work, including embryonic stem-cell culture, could provide alternative solutions for patients. PTI

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Combo Therapy Could Tackle Drug-Resistant Cancer-(ET-17/03/2004)

Using two drugs instead of just one could help cancer patients whose tumors do not respond to standard treatment, researchers said. When they tested the combination therapy in mice with a type of lymphoma that is resistant to standard therapy, it caused complete remission in all the animals. If tests in humans show it is safe and effective, scientists at the Cold Spring Harbor Laboratory in New York believe it could provide a new strategy for overcoming drug resistance in many forms of cancer. "Our results provide in vivo (living) validation for a strategy to reverse drug resistance in human cancers," Scott Lowe, the head of the research team, said in a report in the science journal Nature.

Chemotherapy drugs work by triggering a self-destruct program in cancerous cells but some do not respond to the toxic treatments and continue to replicate and form tumors. Lowe and his team decided to use two drugs to deliver a "one two punch" as in boxing to knock out the drug-resistant cells. They discovered that when they combined the drug rapamycin with the chemotherapy treatment doxorubicin in mice there were massive deaths of lymphoma cells. The tumors disappeared quickly and the mice tolerated the combination therapy well. Mice treated with the therapy had lymphomas which had a protein called Akt that inactivated the cell death mechanism in cancerous cells, which made them resistant to the chemotherapy drugs. But they found that rapamycin blocked the action of Akt and restored the death mechanism which the second drug triggered to deliver the knock-out punch.

Lymphoma includes a variety of cancer of the lymphatic system in the body. It occurs when the cells grow abnormally and out of control. The two main types of lymphoma are Hodgkin's disease and non-Hodgkin's lymphoma. The disease can be treated with surgery if it is confined to one area, radiotherapy, chemotherapy and immunotherapy or a combination of them

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Cancer Deadlier for Poor, Minorities-(HealthDayNews-11/03/2004)

Minorities and people living in poverty are still at greater risk of getting cancer and dying from it than whites and more affluent individuals, a new American Cancer Society study finds. Blacks have the highest death rate from all cancers combined, with an annual death rate from cancer that is 40 percent higher for black men and 20 percent higher for black women than their white counterparts, the study found. Being poor also boosts cancer death rates, regardless of race or ethnicity, researchers found. Men who live in poverty-stricken counties have a 13 percent higher death rate from all cancers combined, vs. men in richer counties. Cancer deaths are 3 percent higher for women in poor counties than for their more affluent counterparts. The report appears in the March/April issue of CA: A Cancer Journal for Clinicians, a peer-reviewed journal of the American Cancer Society. "The issue of how we can actually eliminate these disparities represents a very large and unresolved problem," says Dr. Michael Thun, head of epidemiology research at the American Cancer Society and a co-author of the paper.

Using data from the National Cancer Institute, researchers documented and provided examples of disparities across the entire spectrum of cancer intervention, from primary prevention to end-of-life care. To begin with, the prevalence of certain cancers appears to vary among racial and ethnic groups. Asian-Americans and Hispanic/Latinos, for example, suffer from higher rates of stomach cancer. Access to recommended screenings also varies. Mammography use was lowest among American Indian/Alaskan Native women. Only 52 percent had a mammogram within two years, while just 36.6 percent had one in the last year. Gaps also persist in the availability of quality treatment and the adequacy of pain relief for those who are dying of cancer. Poverty, lack of health insurance, and racism all contribute to the chasm in cancer care, the authors explain. It will take the combined effort of many different groups to narrow the gap, they add. "Communities can do a lot by exposing the efforts of tobacco companies to prey on more vulnerable and less educated segments of the population," Thun says.

Recognizing the challenge, Aetna Inc. last year became the only national health insurer to begin collecting racial and ethnic data from its members. The company says that is part of a larger initiative it has developed to understand differences in disparities in care and develop strategies to reduce the gaps. Already, the Hartford, Conn.-based health insurer has rolled out a program to educate and support black women who are at increased risk of preterm labor. Aetna defends its data collection effort, which critics say raises concerns about patient privacy. "Without data, you're kind of shooting yourself in the dark," says Dr. Melissa Welch, medical director for health-care delivery in Aetna's West region. "The good news is we've at least taken a step." Aetna also has developed a cultural competency module that its physicians and nurse employees are required to take. The goal now is to find a way to expand that training to all network providers, she says.

For its part, the cancer society has set a goal of reducing cancer death rates and incidence by the year 2015. Part of the challenge is to reduce disparities in cancer care. "There is a downturn in death rates from all cancers combined across all racial and ethnic subgroups, so there is progress being made in improving early detection, and there's certainly been progress in treating certain cancers," Thun notes. "It's that the progress is not being shared equally among socioeconomic groups."

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Study Slams Some Alternative Cancer Treatments-(HealthDayNews-12/03/2004)

Several alternative cancer treatments that are often described as unproven have actually been researched and debunked, and they therefore should be termed "disproven," a new report says. Andrew Vickers, an assistant attending research methodologist at Memorial Sloan-Kettering Cancer Center in New York City, evaluated data from clinical trials of several alternative cancer therapies, including Laetrile, shark cartilage and metabolic treatments, among other approaches. Vickers notes many of the treatments he reviewed are no longer available or no longer popular. He defines these alternative therapies as those "that attempt to extend life and are used instead of conventional care such as surgery or radiation. I wasn't looking at complementary therapies. We actually provide those at Memorial Sloan-Kettering. They are used to treat the symptoms of cancer," Vickers says.

For instance, he explains, Sloan-Kettering researchers are studying the value of acupuncture for end-stage cancer pain. "I was looking at therapies that claim to increase your life span," Vickers says. For instance, he reviewed a treatment that's based on the belief that all cancers are caused by a single bacterium. The treatment includes efforts to "detoxify" the immune system through diet and enemas, Vickers says. But when the therapy was compared to conventional treatments, there was no difference in survival between the groups. And those treated at the clinic that offered the therapy had a poorer quality of life, Vickers says. The report appears in the March/April issue of CA: A Cancer Journal for Clinicians.

In the paper, Vickers also refutes chaparral, a desert shrub popular with Native American healers before becoming an anticancer remedy; high doses of Vitamin C; Laetrile, a treatment popular in the 1970s derived from apricot pits; shark cartilage; and other treatments. Vickers also worries about the time and financial costs for patients who invest in the disproven therapies. These costs can run to $60,000 for a six-month course, when expenses such as travel, room and board and pay for a caregiver are tallied up, he says.

Leanna Standish, a senior research scientist and naturopathic physician at Bastyr University in Seattle, praises Vickers' study for its information, but adds "this paper comes at a very late date." Among health-care providers who are trained in complementary and alternative methods (CAM), "it is widely known that the evidence base for these old and out-of-date alternative treatments is very weak indeed," she says. "Who prescribes hydrazine sulfate, high-dose vitamin C, chaparrel or shark cartilage anymore?" Standish asks. She adds that health-care providers might take a moment to explore why cancer patients seek out such treatment. "The reason cancer patients continue to seek CAM is because our current 'proven' therapies for most solid tumors such as lung, breast and colon are still not very effective, have difficult side effects for many, and people are still dying of cancer." Says Vickers: "We discourage people from using alternative cancer therapies. And that would include anything you have to stop conventional care to do."

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Yoga Helpful to Some Fighting Cancer-(ET-13/03/2004)

Many Americans who have cancer have rushed through their daily grind until they are brought up short by a disease which wreaked havoc on their physical and emotional lives. A growing number of hospitals and other organizations are discovering a tranquil 5,000-year-old therapy from India that may help them - yoga. "It's the oldest strategy for stress management," said Debra Mulnick, a registered nurse who offers classes through the Mountain States Tumor Institute at St. Luke's Regional Medical Center in Boise. "Our culture is just starved for the concepts we teach, such as how to be kind to ourselves. When we're tired, we usually just go for a triple latte and go for a run." But cancer and treatments such as chemotherapy and radiation produce such side-effects as fatigue, nausea and pain from surgery. Running after a latte is not in order and even aerobic forms of yoga are not appropriate. Society may look at yoga as a New Age whim, but advocates say that while it may not directly fight a tumor, it does have positive effects which can complement medication.

The American Cancer Society said research has shown that yoga can be used to control physiological functions such as blood pressure, heart rate, respiration, metabolism, body temperature, brain waves and other bodily functions. Stress can weaken the immune system, making it even tougher to battle cancer. Yoga means "union" in ancient Sanskrit, the language the first practitioners spoke, Mulnick said. The many yoga forms can involve stretching and strength exercises, deep breathing, meditation and religious observance. "Ahimsa" means "nonviolence." But that means nonviolence to oneself, Mulnick said. Cancer patients may be extremely fatigued and a hard workout is not workable. She instead emphasizes relaxation and deep breathing. "The goal isn't to reach a physical peak. It's the exact opposite of 'no pain, no gain.' You want to be nurturing," said Debra Murphy, who teaches yoga classes for cancer patients under the sponsorship of McCall Community Hospital north of Boise.The two teachers said they tell participants that if a certain yoga move is painful, they should avoid it.

In Sanskrit, "pranayama" means "science of the breath." Yoga students consciously learn to breathe slowly and rhythmically. Sometimes the only thing cancer patients can do during yoga sessions is breathe deeply, but they can practice it at any time. They can do the same with meditation. The teachers said everyone has a continual internal monologue and the chatter is even worse when they are troubled, such as fighting cancer. Meditation allows them to focus their minds on other things, such as how their bodies feel. "Sometimes, just a minute of not having those thoughts can be a reprieve," Mulnick said. "But the training has been shown to have lasting benefits for days and even weeks. People don't have to be pulled down a path of habitual worrying." Murphy said a McCall psychiatrist visits her sessions to advise the participants in meditation.

"Sangha" means "community." The people in the yoga sessions realize they aren't alone in their cancer experiences. Mulnick said the vast majority in her sessions are women. They can discuss side-effects from breast cancer and medication, such as hot flashes, insomnia and the early onset of menopause. Murphy said one woman who finished cancer treatment found the yoga sessions had become a big part of her life. "She said that when you're undergoing chemo, you feel like 'I've done everything I can.' But when you're done, you're in freefall. You need something to do." Mulnick said she studied for five years under Jnani Chapman, a registered nurse and stress management specialist for the Breast Cancer Program at the University of California, San Francisco. Murphy has a doctorate in exercise science and specializes in adaptive exercise programs. At the country's most prestigious cancer clinics, such as Memorial Sloan-Kettering Center in New York City, rolled-up yoga mats are a common sight. Yoga is routinely prescribed by oncologists for stress and to regain movement. "These programs, more and more, will be part of what is offered," Mulnick said. "Yoga is not ever thought of as in lieu of professional treatment. But it's going to become a standard of care

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A Vaccine Against Cancer?-(ET-01/03/2004)

The success of two recent cancer vaccine trials has focused attention on a growing area of research, using the body's own immune system to fight cancer. It's an approach that could revolutionize cancer treatment, say experts. In a study published in the Journal of the National Cancer Institute (Vol. 96, No. 4: 326-331), researchers from Baylor University Medical Center at Dallas reported that their experimental vaccine caused a complete disappearance of advanced non-small cell lung cancer in 3 patients of 43 who were treated. In 7 other patients, the disease did not progress for a period ranging from 5 months to 28 months, while an eighth patient saw his lung tumor shrink by 30%. The vaccine, called GVAX, was made by altering each patient's own tumor cells to make them stimulate an attack by the immune system against the cancer. This was the first time immune therapy alone has been shown to be effective against metastatic non-small cell lung cancer, said lead researcher John Nemunaitis, MD. And while it's too soon to call this a cure, the results are certainly "promising," he said, for patients with a disease that is frequently resistant to chemotherapy and often recurs even after a tumor is removed.

The second study, published in the British journal Lancet (Vol. 363, No. 9409: 594-599), described results from a Phase III trial of a vaccine designed to prevent recurrence of kidney cancer. Again, the researchers used patients' own tumor cells to create the vaccine, which was given after surgically removing the diseased kidney. Patients who got the vaccine after surgery did better than those who received no further treatment; moreover, it took longer for their cancer to come back, in those cases where it did recur.

Although these and similar trials are not yet conclusive, cancer vaccine expert Jeffrey Schlom, PhD, of the National Cancer Institute, says they are "suggestive of something that's potentially very important. The field is progressing exponentially in terms of knowledge and the types of vaccines that are being used," said Schlom, who heads up NCI's Laboratory of Tumor Immunology and Biology. "This is a very exciting time."

Cancer vaccine research is focused primarily on treating existing cancer, rather than preventing new cases. The idea is to kick-start the immune system so that it attacks tumor cells it would otherwise not recognize as a threat to the body. This is not only a completely different approach to treating cancer, but one that has the potential to be virtually free of deadly side effects, Schlom said. In the lung cancer vaccine trial, for instance, the most common side effect was relatively mild irritation at the injection site. In the kidney cancer trial, which included 177 vaccinated patients, only 12 vaccine-related side effects were noted, and these also were fairly mild. "So far there have been extremely few toxic side effects" in vaccines that have been tested, Schlom said.

Researchers are pursuing numerous avenues in the search for effective cancer vaccines, including using tumor cells or extracts of tumors from each individual patient. In some vaccines these cells are modified by adding proteins or other substances that stimulate the immune system.Another approach involves placing tumor antigens-substances that cause an immune system response-into viruses, which can deliver the antigens into the body very efficiently. "Some of these vaccines are just entering into clinical trials, some have been in trials for a few years, but it takes years to find out if they work," Schlom explained.

Progress is slow for a number of reasons, not least of which is the complexity and delicacy of the immune system. Doctors must tread carefully. "Your body in a normal lifespan has to deal with lots of biological insults-bacteria, viruses, yeast," explained immunologist/microbiologist T.J. Koerner, PhD, scientific program director for the American Cancer Society. "If you disrupted the normal immune system, you might increase susceptibility to other things." Conversely, the immune system might get too revved up and start destroying other cells besides the tumor. Schlom sees another major obstacle to vaccine therapy: the nature of the clinical trials process itself. Any new therapy first has to be tested in patients who have failed all conventional treatments. But this type of trial is a poor setting for testing a cancer vaccine, Schlom said. Because many conventional cancer treatments are toxic to cancer cells and normal cells alike, the immune systems of patients in these trials may be too damaged to respond effectively to the vaccine. Moreover, patients in this situation typically have very large tumors. Not only does a large tumor depress the immune system, it makes any immune response less likely to succeed. Killing 100 tumor cells is far easier than killing 1 billion.

Despite the inherent difficulties involved in the research, both Schlom and Koerner are optimistic. "There's always the hype and the hope associated with the vaccine being a potential cure-all and that's got to be tempered," said Koerner. "[But] I really think that some subsets of cancer will probably be very beneficially treated." But continuing clinical trials of promising new therapies is extremely important to success. Schlom said many cancer centers are conducting vaccine trials, and may be able to point patients to a trial that is right for their particular situation

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New Tumor Marker Found-(HealthDayNews-01/03/2004)

A new tumor marker that's associated with many kinds of cancers, including one-third of breast and colon cancers, has been identified by Boston University School of Medicine researchers. They identified this new tumor marker (absence of SMAD8) using a new university-developed procedure called Targeted Expressed Gene Display (TEGD), which can identify related members of a large family of genes, their variants and their patterns of expression. The research appears in the March 1 issue of Cancer Research. TEGD could prove an important component in the accurate diagnosis of diseases caused by the absence or loss of critical components of the body, the researchers say. Information provided by TEGD could help assess disease prognosis and design customized treatment for patients. "We think that TEGD has the potential to advance the ability to probe gene families for genetic and epigenetic defects to a new level of sophistication and could be adopted for routine use in the near future," study author Sam Thiagalingam, an assistant professor of medicine, genetics & genomics and pathology, says in a prepared statement

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Greek Scientists Find Way to Weaken Cancer Cells-(Reuters-01/03/2004)

Greek scientists said they have found a way to lower cancer cell resistance to medical treatment in what could be a major step in treating a disease that kills more than six million people every year. The procedure, which only recently started testing on animals, could make chemotherapy more effective at significantly reduced dosages and eliminate many of its side effects. The key lies in 'switching off' Apolipoprotein J, also known as clusterin or Apo J for short, a protein used by healthy and diseased cells alike as a shield against attacks, Stathis Gonos, leader of the research team, told Reuters. "Our research was looking at genetic and environmental factors related to aging, and that is how we found the function of Apo J in healthy cells is to act as a shield, or 'survival factor', against toxic factors in the environment," Gonos said. "Our next step was to investigate whether Apo J has a similar function in cancer cells, and indeed saw that it retains the same function of defending cells, shielding them from e.g. chemotherapy prescribed by a doctor to treat cancer," he added.

Cells react to what they perceive as an assault with all the weapons they have, producing vast quantities of Apo J as a shield against the attack, be that an infection or an anti-cancer drug. "We used a new technology called RNA Interference to silence the expression of Apo J and saw that in the case of cancer cells they became a lot more fragile and this made it a lot easier to kill them with normal chemo," Gonos said. "We had spectacular results even when using a tenth of the usual dosage," he added, "and this means that many of the side-effects of chemotherapy will likely disappear as we are able to reduce dosages." Many patients undergoing chemotherapy experience anemia, nausea, hair loss or infection due to low blood cell counts.

The Greek team, who are financed by the European Union, have submitted a global patent application in partnership with Canadian biotech firm OncoGeneX and scientists from the University of British Columbia. They have recently started animal trials at Vancouver General Hospital, with Gonos forecasting human trials to start in between three and five years. According to data from the World Health Organization's World Cancer Report, in the year 2000 alone around ten million people worldwide developed a malignant tumor and more than six million died of the disease

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New Target for Tumor-Killing Drugs Found-(HealthDayNews-26/02/2004)

New research offers evidence that a particular molecule may provide a target for the development of drugs to treat a wide variety of tumors, including some that are resistant to conventional therapies. The research, published online in Cancer Cell, found that the insulin-like growth factor 1 receptor (IGF-1R) is necessary for the survival of tumor cells and that using selective small molecules to inhibit IGF-1R may be a potential anticancer treatment. Many previous studies have suggested that IGF-1R is a factor in cancer development in humans. IGF-1R is present in a broad range of tumor types. But it hasn't been regarded as a likely target for cancer drugs because many normal cells also contain IGF-1R. In this new research, scientists from Dana-Farber Cancer Institute in Boston and Novartis Institutes for Biomedical Research Basel demonstrated that inhibiting IGF-1R had powerful effects against many kinds of cancer cells grown in the laboratory.

The scientists also identified two small molecules that are selective inhibitors of IGF-1R. These molecules offer potential for drug development. "These results suggest that IGF-1R function is critically required for tumor cell survival, but dispensable for survival of normal cells in adult animals," study author Dr. Constantine S. Mitsiades says in a prepared statement. "The preclinical activity of IGF-1R inhibitors against a broad spectrum of tumor cells and, importantly, their ability to sensitize tumor cells to a wide range of anticancer agents, highlight the major role of IGF-1R signaling for human malignant cells, and suggest that the molecular pathway of IGF-1R is an attractive potential target for development of anticancer therapies," Mitsiades says.

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Study Finds Familial Link in Many Cancers-(HealthDayNews-16/02/2004)

A new study finds children of cancer sufferers may face a higher risk for inheriting the same type of cancer their parents had-no matter which type of cancer it was. German and Swedish researchers, looking into cancer incidences among family members, found the average risk that the children would inherit the same cancer as their parent was 5.5 percent. That contrasted with an average 3 percent risk found in the general population. "This applies to all the cancers that we studied. The only connection that we didn't see that was significantly higher were those with a rare form of some cancers of connective tissue," says Dr. Kari Hemminki of the German Cancer Research Center in Heidelberg, Germany. "But generally we saw this link in all the cases."

Even stronger links were seen in several types of cancer. Males, for instance, had a 15 percent chance of getting prostate cancer. All persons whose parents had intestinal cancer had a 10 percent risk, while women had an 8.5 percent risk of breast cancer if their mother had it. Some of the highest genetic risks were found in families with testicular cancer; the sons of affected fathers had four times the risk compared to sons of families without testicular cancer. Moreover, brothers of affected individuals had a nine times higher risk to develop this cancer.

Scientists had previously thought that only certain types of cancer carried a familial link. Hemminki's research, which looked through the Swedish family register, a record of all individuals born in Sweden after 1932 and comprising more than 10 million individuals, showed a link across almost all types of cancer. Hemminki identified almost 5,000 families in which several cases of the same type of tumor occurred-an indicator of familial cancer. Based on the data, Hemminki calculated the familial risks for each tumor type with a high degree of accuracy.

Some caution, though, that environment might also play a role. "The relative risks and types of cancers vary by study. It is assumed that the correlation is a function of shared genetic, environmental and lifestyle risks," says Dr. Mary B. Daly of the Fox Chase Cancer Center in Philadelphia. "As a result, the exact numbers seen in Sweden may be different from those seen in other ethnic groups." Those in families with a known hereditary risk, such as those carrying BRCA1 or BRCA2 genes associated with breast cancer, should visit a cancer risk program, Daly adds. "It is important to note that although the cancer risks are increased in children and siblings of cancer patients, typically two to fourfold, the absolute risk is still quite small for most cancers," says Douglas F. Easton, of Cancer Research UK. "Generally, therefore, no specific action is advised for individuals with just one affected relative." Those with a stronger family history may be referred to a cancer genetics clinic, he says. But one need not worry as much if a relative outside the immediate family is affected, say a grandparent, uncle or cousin. "You only inherit 50 percent of the genes from your genetic relation, so they are diluted quite fast," Hemminki says. The report appeared in a recent issue of the International Journal of Cancer

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Cancer Tumors Clamp Blood Vessels Shut- (HealthDayNews-18/02/2004)

Scientists have now shown that cancer tumors actually clamp internal blood vessels shut, making it difficult for anti-cancer drugs traveling through those vessels to hit home. Counteracting this might make it easier for the drugs to get where they need to go, but it also might open up another avenue for cancer cells to spread, the researchers warn. Drug delivery can indeed be a problem in some cancer patients, says Dr. Jay Brooks, chief of hematology/oncology at the Ochsner Clinic Foundation in New Orleans. Lack of adequate blood flow can also be a big issue for radiation therapy, which requires oxygen to get to the tumor, he adds. "For many years, we've realized that tumors have areas where there are dead cells or blood cells don't adequately feed the centers," says Dr. Len Lichtenfeld, deputy chief medical officer of the American Cancer Society in Atlanta. "We've been trying to find out what we can do to improve oxygenation and therapy directed at cancers by trying to overcome these areas of low oxygen that are present in cancers. It seems intuitive, but this is an actual laboratory demonstration."The demonstration was done with mice, however, which means that much more research needs to be done before scientists can begin to know what the implications are for humans.

Rakesh K. Jain, director of the Steele Laboratory at Massachusetts General Hospital and the lead author of a brief communication on the discovery in the Feb. 19 issue of Nature, likens the process to a garden hose lying on the driveway. If you drive the wheels of the car on top of the hose, the water flow will stop. "That's exactly what cancer cells do to vessels," he says. "They compress many of the blood vessels by proliferating around them." While Jain, who is also a professor of tumor biology at Harvard Medical School, and his colleagues had long suspected this might be the case, they lacked a way to prove it. They needed a drug that would kill only cancer cells and not blood vessel cells. "If I could kill cancer cells around the blood vessels, then the vessels should open up," Jain says.

Eventually, the researchers decided to graft human cancer cells into mice, then treat them with diphtheria toxin, a drug that kills human cells while sparing mouse cells. As expected, the tumor cells started to die off and the blood vessels started to open up and become functional again. But something unexpected also happened (or didn't happen). "The surprise came with the lymphatic vessels," Jain says. The job of the lymphatic vessels is to drain fluid from organs and tumors. In this model, the lymphatic vessels opened up, but they didn't start functioning again. "Apparently, the tumor is somehow irreversibly damaging lymphatic vessels so they are unable to function," Jain says. "We do not yet know how this is happening."

There is another unanswered question: Will restoring blood flow also allow cancer cells to escape and migrate to other parts of the body? "It might also be able to carry cancer cells out and contribute to metastasis," Jain says. "We don't know that yet. That's a worry." The study itself is quite preliminary, and not all tumors behave the same way. "This is a very experimental setting, but there's a whole biology of relationships between blood vessels and lymphatic control with tumors that we're going to be studying and hopefully exploiting," Brooks says

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Radiowave Treatment Provides Cancer Pain Relief-(ET-10/02/2004)

For patients with cancer that has spread to the bone, destruction of tumor cells with a treatment called radiofrequency ablation (RFA) provides significant and lasting pain relief, new research shows. In the study, nearly all patients experienced a major reduction in pain beginning a week after treatment and extending as long as 24 weeks. Radiation therapy is the standard treatment for cancer-related bone pain, the authors explain in the Journal of Clinical Oncology, but as many as 30 percent of patients do not gain relief from such treatment.

Dr. J. William Charboneau from Mayo Clinic in Rochester, Minnesota and colleagues assessed the outcomes of 43 patients who were treated with RFA. All patients had severe bone cancer pain and had either failed or were poor candidates for standard treatments. Each bone lesion required about three RFA applications with a total treatment time of around 49 minutes. "We limited the number of (bone lesions) for the study to know for sure how effective the method was," Charboneau told Reuters Health. "You could do several lesions," he explained, but it would not work for cancer that has spread widely to many sites. "There is a practical limit." Treatment with RFA allowed patients to reduce their use of pain medications. Use of such drugs fell after week 1, the results indicate, but increased again at week 24 despite the maintenance of lower pain scores. "RFA is a highly effective treatment to reduce severe bone pain from a limited number of (sites), and the duration of relief is long," Charboneau said.

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Better Care Urged for Kids Who Survive Cancer-(ET-09/02/2004)

Follow-up of children who survive cancer was called for after British researchers identified significant variations in the levels of long-term care. The Cancer Research UK team sent questionnaires to clinicians involved in long-term follow-up of childhood cancer survivors in the UK and Ireland. They received 71 replies, a response rate of 77 per cent. Of the 71 clinicians, 68 (96 per cent) followed up all survivors in a hospital clinic until at least five years after the end of treatment. Only two reported discharging before this period but always to the patient's GP. After this five-year period, they found that 37 (or 52 per cent) of the clinicians continued to follow all their patients for life, but 32 (or 45 per cent) discharged some of their patients, nearly always to the patients' GP.

Researchers also analyzed preliminary data from the British Childhood Cancer Survivor Study, which is looking at the long-term effect of anti-cancer treatments in survivors of the disease. They contacted some 11,000 general practitioners and asked them whether their patients were on regular hospital follow up. Over 60 per cent of the GPs reported that this was not the case. "It's clear we need a system to improve the implementation of national guidelines, to ensure that survivors don't miss out on long-term surveillance should they require it," said Mike Hawkins, study author and director of the Center for Childhood Cancer at Birmingham University. "Around one in 1000 young adults in the UK is a survivor of childhood cancer, which means they are no longer the tiny minority they used to be," he added in a statement.

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Many Cancer Patients Have Untreated Depression-(Reuters Health-06/02/2004)

One in 12 cancer patients may have depression, which often goes untreated, new research shows. After screening more than 5,000 cancer patients, UK investigators estimated that 8 percent were depressed. However, only half of diagnosed patients had ever discussed their low mood with their doctors, and only 15 percent were receiving proper treatment for depression. Depression is often tackled with a combination of therapy and prescription drugs. In an accompanying study, however, the researchers demonstrate that many cancer patients with depression also appeared to benefit from weekly visits with a specially trained nurse who encouraged them to adopt a positive and proactive approach to their problems and to seek help for their depression. Although doctors may be well aware that cancer patients are at risk of depression, many factors can prevent them from focusing their attention on that aspect of care, study author Dr. Michael Sharpe of the University of Edinburgh told Reuters Health.

For instance, patients may hesitate to mention their mood, oncologists may be too busy to ask, and general practitioners may believe a cancer patient's needs are all being met by a cancer doctor, Sharpe explained. Furthermore, even when doctors notice a patient is depressed, they may consider it to be an "understandable" side effect of cancer, and fail to take it seriously, the authors write in the British Journal of Cancer. "The common factor is that the focus of all concerned is on the cancer - and the depression gets ignored," Sharpe said. He added that he and his colleagues hope that, one day, treatment for depression will become a standard aspect of cancer patients' care, receiving the same attention as other symptoms like pain and fatigue.

During the studies, Sharpe and his colleagues screened 5,613 patients attending an oncology clinic for depression, and asked those diagnosed with the condition about the care they had received. Most of the participants were outpatients with inactive cancer, who were no longer receiving treatment for their disease.

In addition, Sharpe's team asked 30 cancer patients diagnosed with depression to participate in weekly discussions with a nurse about depression and how they can get treatment, and compared their progress to another 30 depressed cancer patients treated by their general practitioners. Over the course of six months, 90 percent of nurse-treated patients but only half of the others were prescribed an antidepressant. By the end of the study, the researchers found that only 5 percent of patients who participated in weekly sessions still had depression, compared with 57 percent of patients whose treatment was left up to their general practitioners. Although there are many possible reasons why patients benefited from speaking with a nurse about their depression, Sharpe suggested that the most important factor may stem from being encouraged to take charge of their lives and problems. "Being helped to get back a feeling of being in control of their lives is a key factor in their recovery," Sharpe noted

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Optimism No Help Vs. Cancer, Study Says-(Associated Press-09/02/2004)

A positive attitude does not improve the chances of surviving cancer and doctors who encourage patients to keep up hope may be burdening them, according to the results of research. Optimism made no difference in the fate of most of the 179 cancer patients that Australian researchers followed over five years. Only eight people were still living by the time the study ended in 2001. All the patients studied were suffering from a common form of lung cancer. Although the study was small and dealt with a kind of cancer that offers little chance for survival (about 12 percent of patients live beyond five years), health experts say it is the first scientifically valid look at optimism and cancer. The results surprised researchers, who expected optimistic patients to live longer than their hopeless counterparts. Patients are burdened by trying to maintain a positive outlook during their difficult situations, said researchers from the Peter MacCallum Cancer Centre in Melbourne, Australia, and five other health centers in an article published in the journal Cancer.

The study found that optimism dimmed when patients experienced the toxic effects of cancer treatment and when they learned more about the realities of the disease. "We should question whether it is valuable to encourage optimism if it results in the patient concealing his or her distress in the misguided belief that this will afford survival benefits," the study's lead author Penelope Schofield wrote. "If a patients feels generally pessimistic ... it is important to acknowledge these feelings as valid and acceptable." Although optimism may not help cancer patients live longer, it can help patients in other ways, according to the American Cancer Society, which publishes the journal Cancer. A positive attitude can help lead to healthier eating habits, stopping smoking, drinking less, exercising more and learning more information about one's disease and treatment options. Cancer patients have learned to live with therapy, avoid fatigue and even have returned to work, said Dr. LaMar McGinnis, senior medical consultant for the Atlanta-based society. "It is disappointing they don't reflect on quality of life," McGinnis said. "We did not have any illusions that optimism influences therapy but we do believe that optimism and hope does influence the quality of life a patient has.

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UK Cancer Death Rate Falls 12 Percent -Scientists-(Reuters-03/02/2004)

The death rate for cancer in Britain has fallen 12 percent in a generation, although the rate of people contracting the disease continues to rise, research published shows. Cancer kills one in four Britons, more than any other disease. But screening programs and improved treatments are helping to reduce mortality rates, scientists at British charity Cancer Research UK said. "Most people rightly no longer view cancer as a death sentence," Professor Robert Souhami told a news conference given by the charity, which compared statistics compiled since 1972. "People talk more openly about cancer today compared with 30 years ago. Today most are aware of how to avoid the lifestyle behaviors that cause the disease, like smoking, obesity and excessive alcohol," he added.

The death rate for cancer has dropped more sharply for men than for women since 1972, falling by 18 percent for men and by six percent for women-giving an average of 12 percent. The charity's scientists said this was partly because men smoked far more heavily a generation ago than they do now, whereas women smoking is a more recent trend. Smoking is linked to lung cancer, which kills more people than any other form of the disease. Yet despite the fall in mortality rates, most people who contract cancer in Britain still die from the disease. Professor Peter Selby, also of Cancer Research UK, said giving people a 50-50 chance of surviving was an important goal. "The survival rate for cancer is roughly 40 percent on average, and the next target is to have half survive. It's within our reach," he said.

However, even though survival rates are rising, more people are contracting the disease in the first place in developed countries as populations become older and so more cancer-prone. "There are still, on average, more than 400 people dying from cancer every day in the UK. The rate of cancer deaths may be falling, but the number of people being diagnosed with cancer is increasing," Professor Michel Coleman told the news conference. Cancer survival rates have improved across Western Europe, Cancer Research UK scientists said, with England, Scotland and Wales lagging slightly behind.

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IIT WAGES NEW BATTLE AGAINST CANCER-(Times of India-11/11/2003)

Cancer has more or less maintained its upper hand in its age-old battle with science. Now, two departments at the Indian Institute of Technology (IIT), Powai, have taken fresh guard on behalf of science, armed with materials as diverse as magnetic nanoparticles and turmeric.

Magnetic Nanoparticles: Led by D. Bahadur, department of metallurgical engineering and material sciences, this research project uses a magnetic field to generate heat and destroy cancer cells in the body - and is the first of its kind in India. "The idea was first suggested in an international scientific paper in 1957, but consequently no work was done on it," said Mr. Bahadur. "Over the last decade, there has been some activity in this field again. But then, scientists talked about using magnetic particles in bulk, which had to be implanted in the cancerous region of the body via surgery and was traumatic for the patient." Mr Bahadur's team is researching the use of nanoparticles instead.

By this method, a suspension of magnetic nanoparticles is created in a biocompatible fluid and this fluid is injected in the cancerous region. Then the cancerous part of the body is placed within an area of copper coils and a magnetic field is created to generate heat. Once, the temperature reaches 42 to 60 degrees centigrade; the cancer cells are destroyed. "The advantage of this therapy is that cancer cells can be destroyed selectively, since cancerous tissues have less blood flow and their temperature rises faster than normal cells," said Mr Bahadur. The team has already successfully developed a biocompatible liquid for the nanoparticles to be injected in the body. This has been tested in-vitro, as well as on mice. Thev have also developed a technique whereby the field turns from magnetic to non-magnetic automatically, thus maintaining the heat at 42 to 60 degrees centigrade (higher temperatures can damage normal cells). "We're now ready for large-scale field trials," said Mr Bahadur "Although this treatment can be used for all types of cancers, initially, we'll be concentrating on external tumours, like breast cancer "

Curcumin method: Led by D. Panda, school of bioscience, this research project is more in its nascent stage. It is based on the knowledge that curcumin, a natural component of turmeric, inhibits cancer cell growth - since it's an antioxidant and prevents oxidation of cellular protein. According to Mr. Panda, this probably explains why the number of cancer cases per thousand people in India is much lower than, say the US, where turmeric isn't a natural part of food. "I started research on curcumin two years ago, without any specific aim in mind. I merely thought that we need to advance from the theory that curcumin retards cancer," said Mr. Panda. "Now that we're sure of exact mechanism by which curcumin breaks down cancerous cells, we're trying to make new compounds using curcumin, and combine curcumin drugs with existing drugs." The main advantage of this turmeric component is its lack of toxicity, which is a problem with any other compound used in chemotherapy. Chemotherapy tends to kill cancer as well as normal cells, leading to a number of its notorious side effects. The use of the relatively harmless curcumin promises to reduce these side effects.

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Synthetic Venom May Relieve Cancer Pain-(ET-06/01/2004)

A synthetic form of sea snail venom can ease pain in cancer and AIDS victims who get no relief from morphine or other conventional painkillers, a study found. Laboratory research has found evidence that the venom that the snails inject to immobilize their prey might have beneficial effects on some heart problems, strokes, central nervous system disorders and other ills. The latest study involved the experimental drug ziconotide, a laboratory-made equivalent of a compound in the venom of the small Conus Magus cone snail, which lives in shallow tropical saltwater. The infusions produced significant relief in patients whose pain did not respond to more conventional drugs such as morphine. Side effects, including dizziness and confusion, were common but can be reduced by fine-tuning the drug dose, said co-author Dr. David Ellis, a medical director of Elan Pharmaceuticals, which makes ziconotide and helped fund the study. "This is a new, promising kind of treatment," said Dr. Jerome Yates, vice president for research at the American Cancer Society. Yates, who was not involved in the study, said thousands of cancer patients suffer from intractable pain and might benefit from the new drug.

Elan is seeking federal approval for the drug, and one of the researchers said he expects it to become commercially available within the year. The study appears in the Journal of the American Medical Association. Medtronic, which makes infusion pumps for delivering painkillers, co-funded the study.

Seeking human uses for animals' defense mechanisms is not new. Other recent efforts include an experimental drug derived from snake venom that has shown promise in treating strokes. The snail-venom research involved 111 patients ages 24 to 85 in the United States, Australia and the Netherlands. All were treated with a small, battery-operated pump implanted in their abdomens and attached to a catheter that delivered continuous medication or a dummy drug into fluid surrounding the spinal cord. Treatment lasted about 10 days; most patients were not hospitalized during that time. The patients rated their pain. Pain relief was moderate to complete in 53 percent of ziconotide patients, compared with about 18 percent of the placebo group. Serious side effects occurred in 22 ziconotide patients and four placebo patients. Subsequent research has shown that starting patients on lower doses reduces the risks, and many have remained on treatment for more than a year, Ellis said. "This gives us another weapon to help deal with those patients who don't respond to the normal, conventional treatments," said Dr. Steven Charapata, a co-author and director of the Pain Institute at Research Medical Center in Kansas City, Mo.

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Veggies May Offer Cancer Cure-(HealthDayNews-13/01/2004)

Another round of healthy applause may soon be due for the likes of broccoli, cabbage, turnips and mustard greens. It's already recognized that these humble vegetables may help prevent some cancers. Now, researchers at Texas A&M University say they may have found a way to derive a cancer cure from these foods. The researchers have patented a new use for derivatives of diindolylmethane (DIM), a natural compound derived from certain vegetables, to treat cancer. "We took advantage of a natural chemical, that research has shown will prevent cancer, and developed several more analogs," chemist Steve Safe says in a prepared statement. "DIM is a potent substance. But we made it even more potent against various tumors," Safe says. In laboratory tests, this chemically altered DIM proved effective in inhibiting the growth of breast, pancreatic, colon, bladder and ovarian cancer cells. Limited trials on rats and mice yielded similar results. "One of the best parts is that this treatment appears to have minimal or no side effects; in the mice trials it just stops tumor growth. The hope now is that the patented chemicals can be developed into useful drugs for clinical trials and then be used for cancer treatment," Safe says.

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Adults don't eat enough fruit, veggies to fight cancer: Ontario survey-(CP-16/12/2003)

As many as 2.5 million Canadians could be at risk of developing cancer because they don't eat enough fruits and vegetables to reap cancer-fighting benefits, don't exercise enough and don't keep their weight in check, suggests a new study by Cancer Care Ontario. And governments should be quick to institute educational campaigns about these preventable deaths, similar to the steps taken in the war against tobacco, authors of the study said. "The typical Ontario diet is one where it doesn't provide optimal nourishment, it's lower in vegetables and fruit, nor do we have the activity levels that we can maintain good health and reduce or risk of cancer," said Ontario Cancer Care researcher and dietitian Melody Roberts, who helped create and carry out the Ontario Nutrition and Cancer Prevention Survey.

The survey found that up to 30 per cent of cancers in Ontario could be prevented if Ontarians ate more fruit and vegetables, got more exercise and kept their weight in check. Another 30 per cent of cancers could be eliminated if smokers quit their habit, the survey said. It also found that 835,000 Ontario adults - more men than women - didn't get even the minimum required amount of fruits and vegetables and exercise, and didn't keep their weight below the healthy body mass index of 25. Applied across the country, disregarding any variation in eating and exercise habits, that number would amount to more than 2.5 million Canadian adults, suggested Dr. Alan Hudson, CEO of Cancer Care Ontario. In Ontario, the provincial government currently spends one per cent of its cancer-fighting funds on prevention and screening, the agency said.

"Cancer Care Ontario needs to pay more attention to (prevention), and governments certainly need to pay more attention to it," said Hudson. "(Ontario Health Minister George) Smitherman is very keen on the prevention side . . . I'm hopeful that while he's the minister of health you're going to see much more emphasis on this side than you have in the past." Provinces across the country have been increasing tobacco taxes to offset health-care costs related to tobacco-caused illnesses such as lung cancer, and to dissuade people from buying the lethal product.Bans on tobacco advertising and television commercials about the perils of smoking are also part of the campaign to help people quit.

Similar steps should be taken to convince people that diet and exercise also have a big impact on fighting cancer, said Terry Sullivan, vice-president of research and cancer control at Cancer Care Ontario. "Fifteen years ago people didn't think we could do anything about tobacco, and somehow we've managed to initiate comprehensive strategies to reduce tobacco consumption," Sullivan said. "We have not organized ourselves in a comprehensive strategy with respect to diet, physical activity, healthy body weight and cancer."

The survey backed its findings by saying cancers of the mouth, throat, esophagus, stomach, colon, rectum, pancreas, larynx, lungs and bladder all have "convincing or probable evidence for prevention by vegetable and fruit consumption." Esophagus, colon, rectum, breast, uterus and kidney cancers seem to be positively affected by maintaining a healthy body weight, and physical activity may combat cancer of the colon, rectum, breast, uterus and prostate. Health agencies recommend that adults eat five or more servings of fruits and vegetables a day, but 40 per cent of adults fail to consume that minimum, Cancer Care Ontario adds. The telephone survey, conducted between June 2001 and May 2002, involved 3,183 Ontario residents ages 18 to 64. Forty-eight per cent of Ontarians surveyed were found to be overweight, with a body mass index of 25 or more. The index - the standard measure for health - is calculated by dividing a person's weight in kilograms by the square of their height in metres. Another 48 per cent of those surveyed said they got less than three hours of physical activity a week, less than the recommended 3.5 hours a week. More residents of northern Ontario than southern Ontario and the Toronto area got the recommended amount of exercise, either at work, doing chores or in their leisure time, the study found. Only 14 per cent of those surveyed got the recommended amount of fruit and vegetables and exercise and maintained a healthy weight

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Exercising More After Cancer Boosts Quality of Life-(Reuters Health-28/11/2003)

Study after study has shown that exercise improves quality of life in people who have survived cancer. Now, a new study suggests that improvements in quality of life are related more closely to whether cancer survivors maintain or increase their physical activity after treatment rather than on a particular amount of exercise. "It doesn't matter how much physical activity a cancer survivor engages in after they are diagnosed in terms of improving their quality of life," lead author Dr. Chris M. Blanchard of the University of Ottawa in Canada told Reuters Health. What's important, he said, is "the positive change they make to their physical activity after diagnosis." Blanchard's team studied the relationship between exercise and quality of life in 352 adults who had survived cancer. People who exercised at least half-an-hour three times a week had a significantly higher quality of life than less physically active cancer survivors, the researchers report in the November issue of the journal Preventive Medicine.

The study also showed that people who maintained or increased their physical activity after cancer had a better quality of life than survivors who became less active. In fact, the change in physical activity was more strongly related to quality of life than survivors' overall amount of activity, according to the report.> "So when it comes to promoting physical activity after a cancer diagnosis in terms of improving quality of life, we can promote that cancer survivors increase their physical activity," Blanchard said. It does not seem necessary to recommend a specific amount of exercise, he said. A person who does not exercise at all may be encouraged to exercise a couple of times a week, while it may be helpful for someone who exercises twice a week to add another session each week, he said. But Blanchard cautioned that the study looked at the relationship between changes in physical activity and quality of life, not the effect of exercise on the odds of cancer returning. "More specific amounts of physical activity may be needed in terms of preventing recurrence," he said. "This is a new area that is currently being explored." Blanchard and his colleagues also point out that more research is needed to confirm the findings.

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Second Cancer Risk After Skin Cancer High in Blacks-(Reuters Health-31/10/2003)

Among people who have had skin cancer other than melanoma, blacks appear more likely than other ethnic groups to develop a second malignancy, new research suggests. Several reports have shown an increased risk of other malignancies in patients with a history of skin cancer. The current findings confirm this association, but, for the first time, also indicate the presence of a racial effect. The results, which are reported in medical journal Cancer, are based on data from more than 90,000 postmenopausal women participating in the Women's Health Initiative Observational study.

A history of non-melanoma skin cancer was reported by 7554 of the women, nearly all of whom were white. Such women were 2.3-times more likely than other women to report a second malignancy, study author Dr. Janardan Khandekar, from Evanston Northwestern Healthcare in Illinois, and colleagues note. However, for those black women who did report having had skin cancer, the odds of having a second cancer were increased sevenfold. Other ethnic groups had risks that fell between these extremes. In terms of cancer types, skin cancer history was most strongly tied to liver cancer, followed by Hodgkin disease, leukemia, and lung cancer, the investigators report. The finding that second cancer risk varied by racial group "may reflect underlying ethnic immunologic differences," the researchers note. "This may be a fruitful area for further research on ethnic-related cancer differences," they add.

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Bone Drugs Delay Problems of Cancer Spread-(ET-30/10/2003)

A class of bone-strengthening drugs can have significant benefits for cancer patients whose disease has spread to the bone, according to a review published in the British Medical Journal (Vol. 327, No. 7413: 469-472). The drugs, called bisphosphonates, significantly reduce fractures, abnormally high concentrations of calcium (hypercalcemia), and the need for radiation (often used to relieve pain). The drugs also delayed the onset of these problems, researchers at London's Royal Marsden Hospital found. "Clearly a reduction in fractures, need for additional hospital treatment, or pain would be expected to improve a patient's quality of life," said lead researcher JR Ross, research fellow and specialist registrar in the department of palliative medicine.

Most of the patients studied had breast cancer that had spread to bones or multiple myeloma, a cancer that begins in bones. Bisphosphonate treatment of patients with these conditions has become standard practice in the United States. Ross and her colleagues analyzed the results of 30 studies of bisphosphonate treatment for bone metastases. The drugs did not help patients live longer, but did help them have fewer complications from advanced cancer. Overall, patients who received the drugs had a 31% lower risk of having a fracture in a vertebra, and a 35% lower chance of breaking other bones, when compared to patients given a placebo. Their risk of hypercalcemia was 45% lower, and their risk of needing radiation treatment 33% lower. Those findings suggest patients with other types of cancer that has spread to the bone could also benefit from this therapy, Ross said.

Herman Kattlove, MD, a medical editor with the American Cancer Society, agreed that the drugs might help a broader range of patients whose bones have been weakened by metastases, but noted that "these situations just haven't been well-studied." Ross' analysis showed that it can take months for these beneficial effects to be seen, although pain relief is usually quicker. Patients had to take bisphosphonates for at least six months to see any decrease in the need for radiation treatment or in cases of excessive calcium. To have an impact on broken bones, patients had to take the drugs for a year. Because of that time frame, Ross and colleagues recommend that bisphosphonate treatment begin at the first indication that cancer has spread to the bone, rather than waiting for symptoms like pain to appear. "To obtain maximum benefit, it's important to continue reloading the bone with the drug," she said.

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Study of Testosterone and Elderly Urged-(AP-12/11/2003)

Thousands of older men turn to that macho hormone testosterone in search of youthful vigor and virility, but scientists issued a big caution: There's little evidence the therapy fights any effects of aging, much less that it's safe. The government is planning to study the already contentious treatment, hoping to save men from the same kind of confusion that has plagued women considering estrogen therapy. Studies should begin in 2005, and until they're done, testosterone use isn't justified except for the relatively few men who have severe deficiencies, cautioned National Institute on Aging director Richard Hodes. The independent Institute of Medicine highlighted the urgent need for research, reporting rapid increases in the numbers of older men using testosterone despite questions about benefit - and the possibility that long-term use could spur prostate cancer. "There are people out there who say testosterone replacement therapy is just wonderful, and others who say it doesn't do any good at all. What we're saying is we just don't know," said Dr. Dan Blazer of Duke University Medical Center, who headed the government-requested institute probe that called for careful, stepwise study to settle the questions.

Testosterone shots, patches and gel are government-approved to treat hypogonadism, where men's bodies make very little testosterone because of damage to the testes or other conditions. But some doctors prescribe testosterone as an anti-aging remedy, too. Proponents argue that men may need replacement as hormone levels naturally slowly drop with age, something they've dubbed andropause or male menopause. In fact, many mainstream medical groups doubt andropause is a real phenomenon. Certainly men don't undergo an abrupt drop in hormone levels, with associated symptoms, like women do when estrogen plummets during menopause, said Dr. William Rosner, a testosterone expert with the Endocrine Society. "I don't know who coined this word, but to my mind it's a disservice," said Rosner, a professor of medicine at Columbia University.

While testosterone production peaks during adolescence and early adulthood, the range of normal production at any age is quite wide. The question is whether decreased libido, frailty or other complaints are driven by dropping levels or inevitable consequences of aging. If declining testosterone plays a role, the question then is whether boosting it helps. The questions in many ways parallel controversy over women's hormone therapy, once considered almost a rite of passage for menopause until a major study recently found that estrogen and progestin use can cause heart attacks, strokes and breast cancer. "We got burned a lot with women" for not having adequate science before millions took hormones, Rosner noted. For men, there's even less evidence on which to base a decision, he added. "Testosterone use should not be taken lightly," agreed the American Urological Association.

Yet demand is rising rapidly, the Institute of Medicine reported. More than 1.75 million prescriptions for testosterone products were written in 2002 - a 170 percent increase from 1999 - for an estimated 800,000 patients. Because only about 5 percent of the 4 million to 5 million men with hypogonadism are thought to be getting treatment, that suggests a lot of testosterone users are in a gray zone. The institute recommended that NIA first hunt for possible benefits of testosterone therapy in a few hundred older men tracked for a year or two. Because prostate cancer is common in older men and no one yet knows if hormone use will spur its growth, men at very high cancer risk or who have enlarged prostates should be excluded. If that research finds possible benefits - such as improved sexual or cognitive function or muscle strength - several thousand men would have to be studied for several years to prove the effects and settle safety concerns, the institute said. The cautions aren't likely to dissuade men convinced the hormone makes them feel better. "I don't think it's a placebo effect," said Joseph Marcklinger, 57, of Sudbury, Mass., who credits testosterone gel with alleviating his depression, enough that he could quit antidepressants. "I have more energy, you think a little bit better, I'm stronger.

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Freedom From the Pain of Cancer-(HealthDayNews-16/10/2003)

Guideline-based care provides better management and control of cancer pain than the more traditional "as-needed" pain control. So says a Duke University Medical Center study in the November issue of the American Journal of Managed Care. Guideline-based pain management involves using a targeted approach to controlling pain through a pre-determined patient treatment plan. Using a mathematical model, the Duke team concluded that kind of pain management provided effective relief in 80 percent of cancer patients, compared to 30 percent effectiveness for "as needed" pain management by non-specialty health-care providers. When delivered by oncologists, "as needed" pain management was effective in 55 percent of cancer patients. The Duke study says guideline-based care costs just a few cents more per month per patient than the "as needed" approach. "Pain is one of the most commonly feared symptoms of cancer," study senior author Dr. David Matchar, director of the Duke Center for Clinical Health Policy Research, says in a prepared statement. "Not all health-care providers are equally trained to assess and manage cancer pain. Guidelines can create a level playing field for everyone," Matchar says.

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Soothing the Nausea of Chemotherapy-(HealthDayNews-15/10/2003)

A drug called aprepitant -- the first in a new class of drugs that interfere with the vomiting reflex -- helps reduce chemotherapy-induced nausea and vomiting in cancer patients. That's the claim of two international studies published online Oct. 14 in the Journal of Clinical Oncology. The first study found that adding aprepitant to standard therapy to control nausea and vomiting proved more effective in controlling those symptoms than standard treatment alone. The study says aprepitant helped reduce nausea and vomiting on the day that patients received chemotherapy and for the following several days. "The nausea and vomiting that occurs 24 hours after receiving cisplatin is particularly problematic for patients, and aprepitant provided a substantial improvement," lead researcher Dr. Paul J. Hesketh, of the Caritas St. Elizabeth's Medical Center in Boston, says in a prepared statement. "Aprepitant should change the standard of care for the treatment of chemotherapy-induced nausea and vomiting, especially for patients receiving chemotherapy drugs known to cause severe vomiting," Hesketch says.

The second study found the benefits of aprepitant extend over multiple cycles of chemotherapy. Previous research found cancer patients experience increasingly severe nausea and vomiting over the course of several cycles of chemotherapy and that standard therapy to control the nausea and vomiting becomes less effective over the course of numerous chemotherapy cycles. The study found that after six cycles of chemotherapy, 59 percent of patients who took aprepitant along with standard therapy reported no nausea or vomiting, compared to 34 percent of patients who received standard therapy alone.

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Study: Cancer Deaths Down-(Yahoo News-11/10/2003)

Fewer people are dying from cancer in Hawaii, according to a new study. The study produced by the American Cancer Society, the Cancer Research Center and the Health Department shows that in the last two decades, about 19 percent fewer Hawaii men and women have died from cancer. "We are doing better," said Dr. Brian Issell, from the Cancer Research Center. "In other words when people get cancer we are able to treat them more effectively." One alarming finding is that lung cancer rates are rising among Filipino men, mainly due to smoking. The study also shows Hawaiian and Filipino women are less likely to come in for life-saving mammograms. The American Cancer Society said efforts like this Hawaii study will go a long way toward helping reach its goal of cutting cancer deaths in half by the year 2015.

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Experimental Cancer Drug Found Less Toxic Than Taxol-(ET-24/09/2003)

American Pharmaceutical Partners Inc. said its experimental cancer drug Abraxane, a re-engineered form of the common chemotherapy drug Taxol, was significantly less toxic and more effective than Taxol itself in late-stage human tests, the Wall Street Journal reported. The company, however, didn't release the data underlying the trial results. The trial also lacked a common safeguard known as double-blinding designed to prevent research bias, since doctors and patients both knew whether Abraxane or Taxol was in use. American Pharmaceutical, Schaumburg, Ill., is one of several concerns racing to modify traditional chemotherapy drugs in ways that limit toxic side effects and improve their tumor-killing power. Many such attempts have fallen flat, although successful Abraxane results could help rejuvenate interest in the field. Some would-be rivals also aren't far behind. Cell Therapeutics Inc, Seattle, is conducting three large-scale trials of a related Taxol derivative called Xyotax in lung-cancer patients, and expects to report its first data by late next year. Further back is NeoPharm Inc., Lake Forest, Ill., which is studying a way of wrapping Taxol in fatty molecules known as liposomes in early-stage trials.

Taxol, known generically as paclitaxel, is a chemotherapy drug widely used to treat breast and ovarian cancer. Like most chemotherapy, Taxol targets rapidly dividing cells, a strategy that kills both tumor cells and some normal cells such as those lining the stomach and colon. The effectiveness of such drugs often is limited by the side effects patients are able to tolerate. Taxol's side effects include nausea, nerve damage and susceptibility to infection resulting from destruction of some blood cells. What is more, Taxol must be accompanied by a derivative of castor oil called Cremophor, which helps the drug circulate through the body. Cremophor, however, is also toxic and can lead to serious allergic reactions.

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Screening Expected to Cut British Cancer Deaths-(Reuters-15/09/2003)

Deaths rates from Britain's biggest cancers should fall within the next decade thanks to advances in screening techniques, the head of the country's largest cancer charity said. Professor Alex Markham, executive director of Cancer Research UK, said improvements in detecting early signs of breast and cervical cancer and the introduction of a screening program for bowel and prostate cancer will improve survival rates. "We are developing new therapies which will revolutionize the way patients are treated in the future, new screening methods to detect early-stage disease and investing more time and energy into helping to prevent the disease occurring in the first place," he said in a statement.

Markham believes extending the breast screening program to women up to the age of 70 will save 600 lives a year and that advances in detecting cervical cancer will mean the disease in picked up in its earliest stages. But he said the biggest improvement will be a screening program for bowel cancer, which is expected to begin within five years and a study that will investigate the best treatment for early prostate cancer. "There are now hundreds of thousands of people alive and well who have survived cancer in this country. They are testimony to the success of research," he said. Although it will take time for the advances to translate into lower death rates, Markham said he believes "it is possible to have cancer under control in this country in the lifetime of my children's children."

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N.Y. Issues First Cancer Prevention Plan-(ET-09/09/2003)

Reducing the number of New Yorkers who smoke, weigh too much, don't exercise enough and are exposed to pollution should be among the state's cancer-fighting priorities over the rest of this decade, a new state cancer control plan stresses. The first-ever state Comprehensive Cancer Control Plan is designed to combat what the authors said is the state's "large cancer burden" - a projected 35,800 deaths in 2003 alone, with the number expected to climb as Baby Boomers continue to age. The study estimated the direct and indirect costs of cancer in the state at $11 billion. "For all its consequence in terms of human suffering and economic cost, there is reason for hope," the plan said. "Cancer is no longer the out-of-control, stealth disease it once was." The plan was devised by state Health Department officials and medical experts under the prodding of the federal Centers for Disease Control, which wants all states to plan cancer prevention and treatment efforts. State Health Commissioner Dr. Antonia Novello met with officials from the American Cancer Society and leading cancer research and treatment facilities in the state to announce the plan and start coordinating its implementation.

"What we basically agreed to do is stay at the table indefinitely," said Dr. David Hohn, president of the Roswell Park Cancer Institute in Buffalo. "This ought to be a living, evolving process and one that we're committed to not having sit on the shelf and gather dust." Donald Distasio, the chief executive officer of the American Cancer Society for New York and New Jersey added: "This has to be real. It's about changing people lives and making their quality of life tremendously better." The plan sets goals for reducing by 2010 behavior that has been linked to cancer, such as smoking and getting too much unprotected exposure to the sun, and increasing beneficial activities such as regular exercise and eating at least five servings a day of fruits and vegetables. It also advocates for more extensive testing to catch cancers earlier and for making both screening and cancer treatments available to more New Yorkers. The study says about a third of all cancers contracted by New Yorkers are preventable.

Some environmental and health groups complained when a draft of the control plan surfaced in June. It contained one reference to environmental factors such as chemical pollution and auto exhaust, which it said "may" be linked to cancer. But the final plan says exposure to some chemicals is known to cause cancer or is likely to do so, including benzene, dioxin and chromium. It also says diesel emissions are "likely" cancer-causing agents, too. "I think that environmental issues very much need to be on the table," Distasio said. "It's a complicated issue, but we are not in any way, shape or form dismissing it."

In addition to Hohn, representatives from Mount Sinai Hospital, the Sloan-Kettering Cancer Center, the University of Rochester's James Wilmot Cancer Center, the NYU Cancer Institute, the Albert Einstein College of Medicine and Glens Falls Hospital attended the meeting with Novello. The experts said afterward they had agreed to work more closely together to attract research and grant dollars for their cancer-fighting efforts.

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"Smart Bomb" Treatment Hones in on Cancer Cells-(HealthDayNews-08/09/2003)

A new treatment that may precisely attack cancer cells like a "smart bomb" has been developed by scientists at Rutgers University in New Jersey. The scientists say their combination of a novel cancer cell-killing agent and a precision-targeting technology shows great potential. The Rutgers approach uses a prodrug to deliver their potent cancer-killing compound to the target. A prodrug is an inert chemical derivative of a drug that can be activated once it reaches its destination inside a patient's body. Prodrugs are able to safely transport highly potent medicines through the body without harming other body tissues along the way. The research was being presented Sept. 8 at the national meeting of the American Chemical Society in New York City.

Traditional anticancer drugs use accelerated cell growth as their trigger. However, this can lead to collateral damage in rapidly replicating normal cells, leading to side effects such as hair loss, nausea and reduced immunity. With the new Rutgers treatment, the prodrugs use an enzyme called nitroreductase as the activating trigger. That guarantees a direct hit on cancer cells. When the gene for this enzyme is inserted into cancer cells, the cancer cells start to express the nitroreductase, marking themselves as targets. The prodrug "bomb" finds these cancer cells and unleashes its cancer-killing toxin. The Rutgers scientists say there is still much research to be done. If all goes well, human clinical trials may begin in a couple of years.

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Common Gene Implicated in Many Cancers-(HealthDayNews-28/08/2003)

A study showing that a relatively common genetic mutation increases the risk of many kinds of cancer points toward a future in which routine screening tests could become a common weapon against cancer, researchers report. The study is part of an important shift in emphasis in research about the role of genetics in cancer. Until recently, researchers have concentrated on what are called "high-penetrance" genes, relatively rare mutations that greatly increase the risk of specific cancers. Now they are looking at more common "low-penetrance" genes that somehow interact with environmental factors to increase the risk of many different cancers.

The new study, reported in the Journal of Clinical Oncology by researchers at Northwestern Memorial Hospital in Chicago, says a mutation in a gene for a protein called transforming growth factor beta (TGF-beta) increases the risk of all cancers by 26 percent. The TGF-beta mutation may increase the risk of breast cancer by 48 percent, ovarian cancer by 53 percent, and colon cancer by 38 percent, the researchers say, with comparable increases in other malignancies. Those risk estimates were produced by amassing data from seven studies that looked at the incidence of the TGF-beta mutation in more than 2,000 patients with many kinds of cancer, says study author Dr. Virginia G. Kaklamani, an oncologist at Northwestern Memorial. The TGF-beta mutation is an obvious candidate for a cancer risk factor because the gene plays an important role in "a pathway that is important in cancer development in general," says Kaklamani.

"In normal cells, it inhibits growth. When normal cells become transformed to cancer cells, the mutation we are talking about decreases that signal, so that it acts as a growth factor." After animal studies showed the mutation played a role in many cancers, Dr. Boris Pasche, then at Memorial Sloan-Kettering Cancer Center in New York City and now at Northwestern, began the analysis of human studies that resulted in the new report. Now the Northwestern researchers are doing studies in which carriers of the mutation are being identified and followed to determine their risk of cancer. "In the future, we hope that we can identify individuals at high risk because they carry the mutation," Kaklamani says.

The ultimate goal is to develop a model that includes a large number of low-penetrance mutations and would assess overall cancer risk with a single genetic test, she says. It's a long-term goal, says Dr. Loren S. Michel, a research fellow at Memorial Sloan-Kettering and a member of the research team, because "finding these common genes has not been easy." The new study is important because it is one of a very few that have identified low-penetrance candidates, he says. That is not an easy job, he says. First comes laboratory work in which "one does a lot of DNA sequencing and tries to find polymorphisms [mutations] that predispose to cancer," Michel says. "Then you go through a huge number of patient samples and find whether this gene is at a very high frequency in a cancer population and in people who do not yet have cancer." The effort is being pushed in a number of laboratories because "finding these genes is going to be the frontier in cancer biology, giving us a new understanding of how cancer develops," Michel says.

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Wrist Bands Can Ease Cancer Nausea, Especially for Patients Who Expect Them to Work-(ET-28/08/2003)

Cancer patients who expected acupressure wrist bands to ease the nausea they have from chemotherapy were much more likely to gain relief than either patients who were not given the bands or those who received them but didn't expect them to help. That's the word from researchers at the James P. Wilmot Cancer Center, who carried out the largest scientific study yet of two products that some believe can reduce nausea. The results, which researchers say point to the power of the placebo effect, were published in Pain and Symptom Management.

Scientists at the cancer center at the University of Rochester Medical Center compared the response in 700 cancer patients who received either two acupressure bands, an acustimulation band, or no band. Both the pressure and the stimulation bands are worn on the wrist, and several studies have shown them to be helpful in reducing nausea from seasickness, motion sickness, and morning sickness from pregnancy. The pressure band applies steady pressure to an acupuncture point on the inside of the wrist; the acustimulation band gives a mild electrical pulse to the same point. Such bands are sold at some drugstores but are not widely used in medicine. Participants in the study wore the bands on the day of their chemotherapy treatment and the following four days. About 85 percent of the study participants were women being treated for breast cancer; most of the others had lymphoma or Hodgkin's disease.

Overall, acupressure patients reported 15 percent less nausea on the day of treatment, compared to patients who wore no band. Acupressure patients had roughly the same amount of nausea and vomiting as the others in the days following treatment. When scientists analyzed the results more closely, they found that the acupressure bands were more helpful to patients who expected the device to ease their nausea. Patients who expected the bands to help rated their nausea 25 percent less severe than other patients on the day of treatment and approximately 13 percent less severe on subsequent days. They also reported having a higher quality of life on those days, and they used less anti-nausea medication. Acupressure patients who did not expect the bands to work did not show any benefit.

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Bone Drugs Stop Cancer-Related Fractures-(Reuters Health-29/08/2003)

A group of bone-strengthening drugs called bisphosphonates can prevent fractures and other skeletal problems in cancer patients, new research shows. Many different types of cancer can spread, or metastasize, to the bone. When this happens, the bone becomes weaker and more likely to break. The new findings are based on a review of 30 studies that looked at bisphosphonate treatment of patients with cancer that had spread to the bone. The report is published in the British Medical Journal.

Treatment with a bisphosphonate (Fosamax and Didronel are examples) for at least 6 months reduced the risk of fractures by 35 percent, study author Dr. Joy R. Ross, from the Royal Marsden Hospital in London, and colleagues report. No benefit was seen when these drugs were taken for less than 6 months. Bisphosphonate therapy also reduced the need for radiation treatment. Moreover, when a fracture did occur, it tended to happen later in patients who were treated with a bisphosphonate rather than nothing at all. There was also evidence that long-term treatment with bisphosphonates reduced the need for orthopedic surgery, the investigators point out.

Despite these encouraging findings, bisphosphonate therapy did not increase the lifespan of cancer patients or prevent spinal cord compression, a potentially serious nerve injury that can cause numbness and weakness in the arms or legs. Although the best drug remains to be determined, in the current study, the most effective bisphosphonates appeared to be the injected ones rather than those taken by mouth, the researchers state. "Further research is need to determine the optimum regimen required to treat patients with bone metastases," the authors state.

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Hispanics Have Unique Cancer Risks-(HealthDayNews-19/08/2003)

Hispanics, the fastest growing minority in the United States, have a unique cancer risk profile that requires a targeted approach to prevention, says an American Cancer Society report. Hispanics are less likely than whites to develop and die from the most common kinds of cancer, but they have higher rates of some other kinds of cancer and are more likely to have cancer diagnosed at a later stage, the report says. The report, which appears in the July/August issue of CA: A Cancer Journal for Clinicians, says that, compared to Caucasians, Hispanics have lower incidence and mortality from all cancers combined, as well as from each of the four most common cancers -- lung, breast, colon and prostate; have higher rates of some other kinds of cancers, including cancers of the stomach, liver, cervix and biliary tract; are less likely to use screening tests for colon, prostate and cervical cancer; have higher rates of overweight and lower rates of physical activity, factors increasingly associated with cancer; have traditionally been much less likely to smoke.

As a group, Hispanics have different cancer risks and rates compared to other ethnic groups. Because of that, Hispanics require different cancer prevention methods. "All of the approaches that are most important in the general population -- preventing and treating tobacco dependence, increasing access to high quality cancer screening and appropriate follow-up care, increasing physical activity, maintaining a health body weight, etc. -- are important for Hispanics," Dr. Michael J. Thun, the American Cancer Society's vice president for epidemiological and surveillance research, says in a news release. "In addition, several other approaches are particularly important for this group: maintaining the frequency of Pap testing, vaccination for hepatitis B, removing barriers that interfere with access to high quality screening and medical care, and forming partnerships to deliver health messages more effectively," Thun says.

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Cancer Rates Decline in European Countries-Study-(Reuters-28/07/2003)

European Union efforts to cut expected deaths from cancer by 15 percent by 2000 fell short of the mark but most countries show declining trends, researchers said. Medical experts had predicted cancer deaths in the European Union would rise to 1.03 million, but the number is closer to 940,500, according to the latest figures from the European Institute of Oncology in Milan, Italy. "Although we fell short of our ambitious target, the reductions are noteworthy," said Professor Peter Boyle, the director of epidemiology and biostatistics at the institute. "With few exceptions most countries are experiencing declining trends in cancer death rates, which seem set to continue, at least in the near future," he added in a statement.

The Europe Against Cancer program was launched in 1985 to combat the disease. In 1986 it prepared a detailed action plan to cut the expected number of cancer deaths by 15 percent by 2000. Although the number of deaths over 15 years has risen by 12 percent in men and nine percent in women, the increase is only about half of what researchers had expected. Luxembourg had the biggest decline in expected deaths with a 24 percent decrease, followed by Finland, Britain, Austria, the Netherlands and Italy. Portugal with 17 percent and Spain with 11 percent had the biggest gains in the research reported in the journal Annals of Oncology. Austria, Finland and Luxembourg had the most effective program for reducing expected cancer deaths in women and Greece and Portugal had slight increases.

Boyle stressed that smoking had a major impact on the Europe Against Cancer program missing its target. "Nine out of 15 countries experienced declines of more than 10 percent in risk of death from all forms of cancer when lung cancer was excluded," Boyle said. "However, the risk of dying from lung cancer in women increased substantially in every country," he added.

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UIC Researchers Pinpoint Genes Involved in Cancer Growth-(ET-23/07/2003)

In a study made possible by the sequencing of the human genome, scientists at the University of Illinois at Chicago have identified 57 genes involved in the growth of human tumor cells. Some of these genes appear to be linked with the growth of cancerous cells only -- not healthy cells -- making them possible targets for new drugs that could halt the spread of disease without necessarily compromising normal processes. Results of the study appear in the July 22, 2003, issue of Cancer Cell.

The research relied on a strategy pioneered in the laboratory of Igor Roninson, distinguished professor of molecular genetics in the UIC College of Medicine. The strategy involves cutting human DNA into tiny, random fragments, inserting the fragments into a mammalian cell using a vector, or delivery vehicle, and inducing them to express their genetic information. Some of the fragments prove to be biologically active by interfering with the function of the genes from which they are derived. In the new study, certain fragments inhibited the multiplication of breast cancer cells by shutting down the genes necessary for cell growth. The experiment enabled researchers in Roninson's laboratory, led by research assistant professor Thomas Primiano, to locate 57 genes involved in cell proliferation. They identified the genes by matching the growth-inhibiting fragments with sequences in the human genome. "Our strategy was validated by the fact that more than half of the genes we identified were already known to play key roles in the growth of cells or the development of cancers," Roninson said. "Many of the other genes, however, were not previously known to be involved in cell division and proliferation. In fact, the functions of some of these genes were entirely unknown."

Analysis of animal studies conducted by other investigators allowed Roninson's group to determine which genes were likely involved in the growth of tumor cells but not normal cells. In so-called "knockout" mice, 20 of the genes the scientists identified as essential for the growth of breast cancer cells had previously been disabled. Lacking any of six of these genes, the animals died in utero. But mice missing any of the other 14 genes matured to adulthood, suffering only limited problems in specific organs. "Obviously, the best drug targets would be genes that are needed only by cancer cells," Roninson said. One of the genes the UIC researchers identified manufactures a protein found on the cell surface called L1-CAM, which is involved in the development of the nervous system and was not previously known to play a role in cancer cell growth. Using antibodies to L1-CAM to disturb its function, the researchers stopped the growth of breast, colon and cervical cancer cells in a petri dish, but left unimpaired the growth of normal breast tissue cells and fibroblasts, which make up connective tissue. This final experiment, Roninson said, confirmed the value of his team's study. "One of the main reasons for sequencing the human genome was the hope that this knowledge would help scientists find molecular targets for new and better medicines," Roninson said. "The genes we have identified clearly have the potential to serve as targets for novel therapeutics in the fight against cancer."

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New Test May Improve Cancer Detection-(Reuters Health-17/07/2003)

A new blood test could represent a simple, inexpensive way of detecting cancer early, new research suggests. The test involves a search for pieces of DNA that are abnormally long. When normal cells in the body die, they release pieces of DNA into the blood. It turns out that dying cancer cells do the same thing, except that the pieces are much longer. By testing for these longer pieces of DNA, doctors could, in theory, detect cancers at an early stage when they are still curable.

Dr. Ie-Ming Shih and colleagues, from Johns Hopkins University in Baltimore, used the new test on 61 patients with gynecologic and breast cancers and on 65 people without cancer. The authors' findings are published in the journal Cancer Research. The test only detected about two-thirds of the patients with cancer, but if the test said that a person had cancer then invariably they did. Moreover, the test was consistently able to discriminate cancerous gynecologic problems, like ovarian cancer, from benign problems, such as cysts. Before the test is ready for clinical use, several issues must be addressed, the authors state. One major concern is that it missed about a third of the people with cancer. However, this could be improved by modifying the test or by combining it with other tests, they add.

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Modified Tetracycline May Help Prevent Cancer Recurrence-(ET-15/07/2003)

Building on previous research, University of Iowa scientists have discovered that a drug already being tested as an anti-cancer agent could potentially be used in conjunction with other cancer therapies to reduce the likelihood of cancer recurrence by targeting the tumor microenvironment. UI scientists in the laboratory of Mary Hendrix, Ph.D., the Kate Daum Research Professor and head of anatomy and cell biology, previously discovered that aggressive tumor cells can modify their local environment and can induce less aggressive tumor cells encountering this modified environment to become more aggressive. This suggested that in addition to treating tumor cells, changes to the surrounding tissue caused by an aggressive tumor should also be treated to reduce the likelihood of recurrence.

In a study, which appears in the November 2002 issue of the journal Molecular Cancer Therapeutics, the UI researchers demonstrate that a chemically modified tetracycline called COL-3 is able to prevent the altered cellular environment from inducing less aggressive cancer cells to behave more aggressively. In their earlier studies, the UI team discovered that aggressive melanoma cells produce a molecule called laminin 5 gamma 2 chain and deposit it into their local environment. Enzymes known as matrix metalloproteinases (MMPs) breakdown the laminin molecules and the resulting fragments act as signaling molecules. Less aggressive melanoma cells respond to these signaling fragments and become more aggressive. The fragments of laminin laid down in the environment by the aggressive tumor cells persist in the environment long after the aggressive cells have gone and affect the less aggressive tumor cells that move into the altered environment. "Standard cancer treatments aim to remove or destroy aggressive cancer cells," said Richard Seftor, Ph.D., lead author of the study and a UI research scientist in Hendrix's lab. "However, we also need to be concerned by the environment left behind by the aggressive cells. We may also need to block these environmental cues."

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More Evidence Chemo During Pregnancy Can Be Safe-(Reuters Health-01/07/2003)

A woman who was diagnosed with cancer and given chemotherapy while she was pregnant has given birth to a healthy child, according to her doctors in Germany. They say the case adds to growing evidence that chemotherapy during pregnancy is safer than many doctors and patients assume. Dr. Holger Stepan, a consultant in the department of gynecology and obstetrics at Leipzig University Clinic, told Reuters Health that the 24-year-old patient was diagnosed with Hodgkin's disease during her 28th week of pregnancy. "At that point we had to weigh the risk of delivering the baby immediately, with all the risks associated with a premature delivery ... against the risks of starting a course of chemotherapy during pregnancy, but with the advantage for the child of being able to prolong the pregnancy," said Stepan.

In her 32nd week of pregnancy, the patient was started on a low dose of chemotherapy with four drugs. "The patient responded well to the therapy," Stepan said. Then at week 34, the baby was delivered by Cesarean section and found to be healthy. The mother then went through a course of high-dose chemotherapy and subsequent radiation, and has since fully recovered with no traces of the cancer left. Stepan said this case adds to the growing body of evidence that patients and doctors may overestimate the risks of in-utero exposure to chemotherapy. He said some types of chemotherapy can be given in the second or third trimester without the risk of fetal malformations -- though he pointed out that chemotherapy does pose such a risk in the first trimester.

Previous research has suggested that once the fetus is 12 weeks or older, the mother can undergo chemotherapy without an increased risk of birth defects or mental impairment. Hodgkin's disease is the most frequent form of cancer among pregnant women after breast cancer, cervical cancer and the skin tumor melanoma. Stepan said the incidence of cancer among pregnant women might increase because many women are now waiting until later in life to have children.

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Help for the Fatigue of Cancer-(HealthDayNews-25/06/2003)

A once-a-month dose of the drug Aranesp corrects anemia in cancer patients who aren't receiving chemotherapy. So says a study in the June 16 issue of the British Journal of Cancer. The findings of this Phase 2 study are notable because cancer patients not receiving chemotherapy usually visit their doctors only once a month. Being able to dose this drug once a month reduces the burden of frequent clinic visits for the patient and doctor. The study was led by Dr. Robert E. Smith, director of the Cancer Treatment and Research Institute, Baptist Medical Center, and a clinical associate professor at the University of South Carolina School of Medicine.

Anemia is a common problem in cancer patients receiving chemotherapy. But many cancer patients also suffer anemia due to the disease itself. Even though it's common and causes symptoms such as severe physical and mental exhaustion, anemia in cancer patients is under-recognized and under-treated. Currently, blood transfusion is the only U.S. Food and Drug Administration approved treatment for cancer-related chronic anemia

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The Single-Minded Sleuth-(ET-20/06/2003)

Twenty years ago biologist Napoleone Ferrara discovered a mysterious protein in the pituitary gland of cows that seemed to make blood vessels grow. He foresaw a new weapon against cancer--block the protein and tumors may be unable to proliferate--but the finding was so obscure that even his boss was skeptical. Last month the drug that resulted from Ferrara's work began to look like a success: Genentech unveiled trial results that showed it extended colon cancer patients' lives by a median of five months, or 30%, one of the bigger advances in years. The drug, Avastin, could hit the market by year-end, joining existing anticancer chemicals and radiation as standard therapy for colon cancer--and it could end up working against other cancers.Thus, Avastin, which blocks VEGF, the protein Ferrara first isolated, could become the first entry in a new way to treat cancer--antiangiogenesis, which shuts down tumors by quelling their ability to form the new blood vessels that feed their expansion.

"It is a big achievement," says Judah Folkman of Harvard's Children's Hospital Boston. He was an early proponent of antiangiogenesis and is known for the experimental drugs angiostatin and endostatin.

During a two-year postdoctoral stint doing biology research at the University of California, San Francisco, Ferrara was handed the low-priority task of exploring the basic science of the pituitary gland. That meant frequent treks to the slaughterhouse to collect cow samples. One day he mixed follicular cells (an extract from the cow pituitary) with blood vessel cells. To his great surprise, the blood cells started multiplying like mad. He theorized that the pituitary cells were secreting a protein--some unknown elixir among several thousand proteins the organ churned out--that instructed blood vessels to sprout tendrils. Skeptical colleagues believed he had merely rediscovered the well-known fibroblast growth factor. Ferrara couldn't prove otherwise because he wasn't able to isolate the protein and lacked enough evidence to publish his theory. But his gut told him he was right, so he scrapped plans to begin an obstetrics practice in Sicily, instead staying in San Francisco to devote himself to research.

Though he was hired by Genentech in 1988 to work on a pregnancy drug, he concentrated on the tedious work of isolating the cow protein that he had stumbled upon years earlier. Driven by the idea that he might discover something totally new, he labored nights and weekends for months, filtering out thousands of other proteins until he finally separated the right one in 1989 and cloned the human version of the gene that produces it. He named it Vascular Endothelial Growth Factor, or VEGF, for its ability to act as a molecular fertilizer for blood vessels while having little effect on other tissues. He realized, five years before Harvard's Folkman would discover angiostatin, that blocking VEGF with a specially tailored drug might lead to a totally new type of cancer therapy.

Ferrara's team and others showed that many tumors secrete large amounts of VEGF to spur nearby blood vessels into growing new branches to supply the tumor. The more VEGF a tumor contains, the more it is likely to grow. By 1993 Ferrara's Genentech colleagues had engineered a monoclonal antibody that latches on to the VEGF molecule and disables it so it can't dock onto its receptor in blood vessels. The antibody dramatically slowed the growth of tumors in mice, but persuading executives to launch costly human trials was a struggle. At the time Genentech focused on heart disease, not cancer. Ferrara kept coming back at them with more data. "He is kind of unstoppable," says Hillan. "He keeps pushing and pushing his ideas," until they prevail.

Human trials of Avastin began in early 1997 and proceeded with little fanfare until mid-1998, when Harvard's Folkman landed on the front page of the New York Times. A media frenzy ensued over Folkman's success at wiping out tumors in lab mice. Ferrara's bosses fretted over whether Genentech was pursuing the right strategy. He urged them to stay the course, noting that the mechanism of Folkman's drugs was unclear and that the results hadn't yet been reproduced. Sure enough, it took years to reproduce those animal findings, and angiostatin and endostatin have been delayed while their backer EntreMed looks for a new partner.

Initial trial results for Avastin in colon and kidney cancer were promising, prompting Genentech to start large-scale tests. But Avastin failed to help breast cancer patients in a study of 462 women completed last fall. Many analysts wrote off the drug entirely. Ferrara felt as if he'd been punched in the stomach. Everything now was riding on the big colon cancer trial, with results due in May 2003. As the outcome neared, Ferrara found it harder to sleep. He was in Italy on May 18 when he received an urgent message to call Genentech Chief Arthur Levinson. He expected mixed news at best. Levinson told him to sit down: The drug had far exceeded expectations. Ferrara, feeling a wave of relief, was speechless.

Ferrara hopes Avastin is just the start. He has been mulling other diseases involving VEGF, including eye problems characterized by a proliferation of blood vessels. Genentech is testing a derivative of Avastin, rhuFab V2, in patients with macular degeneration, a leading cause of blindness. It is now in final-stage human tests. Some 25 trials of Avastin are under way, targeting tumors of the kidney, lung, pancreas and liver. VEGF research has become a cottage industry, with hundreds of new studies emerging every year. Resulting drugs could help heal severe wounds and treat heart and liver diseases. Back in his lab Ferrara is working furiously to figure out how tumors can become resistant to Avastin. One theory, which may explain its failure against breast cancer, is that there may be tissue-specific proteins that spur tumor growth in the absence of VEGF. "This is a long-term quest, and we can't assume that blocking VEGF alone will be enough," he says.

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Cancer Patients Can Beat Depression-(ET-08/06/2003)

Being diagnosed with terminal cancer can bring a flurry of emotions: sadness, fear, anxiety about treatments, concern for loved ones. While such feelings are common and understandable, some patients are so affected by their diagnosis that they develop clinical depression, a sense of hopelessness and loss of pleasure in almost all activities. A new study offers some relief for these patients. Researchers from M.D. Anderson Cancer Center in Texas and the Hoosier Oncology Group in Indiana have found that commonly prescribed antidepressant medication can relieve symptoms of depression in terminally ill cancer patients, and improve their quality of life. The finding is significant, said lead researcher Michael Fisch, MD, of M.D. Anderson, because there is currently no widely accepted way for cancer professionals to deal with depressed patients. "This is a small step to understanding what can be done by an oncologist in the real world," he said.

Many people -- even some patients themselves -- think it's "appropriate" to become depressed after a diagnosis like terminal cancer, said Joy Fincannon Carter, RN, an associate medical editor with the American Cancer Society whose specialty is in psychiatric nursing "You are sad about having cancer, but being sad and having depression are two very different things," she noted. "It's a myth to say that someone who has advanced cancer feels hopeless. Most people don't give up." Instead, their hope focuses on different things, she said. They may look forward to seeing their grandchild participate in a particular event, or take greater joy in visits from friends and family, for instance. But for about 25% of cancer patients, clinical depression is a real problem, and one that is often overlooked.

Oncologists may not recognize the symptoms of depression as clearly as a psychiatric professional would. Many of the physical symptoms of depression, such as loss of appetite, weight fluctuations, or fatigue, are also common side effects of many cancer treatments and may be attributed to that, rather than to a psychological disturbance. Another potential problem is patient-doctor communication. Patients may not discuss feelings of depression with their cancer doctors, and doctors may not ask about it. Even when a patient is recognized as having trouble with depression, it may be difficult to get treatment -- they may feel too sick, there may be insurance issues, or they may not have timely access to mental health specialists.

Fisch and his colleagues tested a simple way for oncologists to recognize depression in their patients, and help them overcome it. The doctors asked their patients two questions to assess their level of depression: "During the past month have you been bothered by feeling down, depressed, or hopeless?" and "During the past month, have you often been bothered by having little interest or pleasure in doing things?" The questions have been used in other psychological studies, Fisch said. The researchers identified 163 patients with symptoms of depression, all of whom had advanced, incurable cancer, and an expected survival between three months and two years. For 12 weeks, half the patients took a standard 20 milligram dose of fluoxetine (Prozac) every day; the rest took a placebo pill. They were questioned about their quality of life and depression every few weeks during the study. The patients on Prozac showed significant improvement in their quality of life and in relief from depression, compared to patients on placebo. Patients who had higher levels of depression were helped the most.

The study shows that the problem of depression can be addressed, even if it's caused by a life-threatening diagnosis, Fincannon Carter said. Effective treatments, such as the fluoxetine studied by Fisch, mean patients don't have to suffer from depression while they're fighting cancer. And, treatment benefits not just the patients, but also their families and caregivers, she added. The work also shows that the cancer care team can take a role in lifting the depression, Fisch said. "The people in that immediate circle of cancer care are the ones who are going to have to screen and have some game plan for what to do." But he stressed that more research should be done to refine the ways the medical community handles depression in cancer patients.

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New Compounds Trigger Cancer Cell Suicide-(Reuters Health-10/06/2003)

Scientists believe they have found a new way to get tumor cells to self-destruct, a discovery that may eventually lead to better drugs to fight cancer. Dr. James A. Wells and Jack T. Nguyen, researchers at Sunesis Pharmaceuticals, Inc., in South San Francisco, California, found two synthetic compounds that triggered programmed cell death, or apoptosis, in cancer cells. Normal human cells only last for so long before a chemical program switches on and kills them. This prevents uncontrolled cell growth and keeps the body in good working order. But in cancer cells, the mechanism is often faulty, and the cells don't die. "We were looking for things that would induce cell death," Wells told Reuters Health. "We took a cell, a whole cell, and we basically punctured the membrane, and then we took the goo out of the cell, and then we screened the goo against the small-molecule library," he said. The small-molecule library was a set of roughly 3,500 compounds. Two of the compounds triggered apoptosis, according to a report in the online Proceedings of the National Academy of Sciences.

The researchers knew they had found what they were looking for when they detected an enzyme called caspase-3. "Caspase-3 is the actual henchman that goes around and executes the cell," Wells said. The compounds were tested on whole normal cells and a variety of cancer cells -- including breast, lung, ovarian, skin and leukemia tumor cells. One of the compounds triggered apoptosis in the cancer cells while having little effect on normal cells. It appeared to be most effective against the leukemia cells. The other compound wasn't as potent in whole cells, although it was potent in the other tests. The researchers speculate that it had difficulty passing through the cell membrane.

The study shows that these compounds might work against cancer cells that are resistant to other cancer drugs. Some chemotherapy agents now in use target a gene called p53, which regulates cell growth. But in many cancer cells, p53 is mutated, so drugs aiming to trigger apoptosis by that route don't work. The research seems promising, but it could be several years before any new cancer drug comes from it. "These compounds should be considered as very early leads. They would need a lot more work," Wells said. "Going forward, we would be enhancing the potency of the drug-like properties of the molecule, and studying the molecules in animals."

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Americans Confused About Cancer Prevention: Survey-(Reuters Health-04/06/2003)

Most Americans know there are ways to lower their risk of cancer, but many are confused about how to do it, according to a survey released at a major cancer meeting this week. Among the 1,000 adults surveyed, the majority recognized that diet may play a role in cancer, but only 38 percent "strongly" agreed that they could reduce their cancer risk by eating a diet high in vegetables, fruits and fiber -- even though there's evidence that such healthful eating habits can cut the risk of some cancers.

Only about half of Americans surveyed agreed that they could reduce their risk of developing certain cancers with exercise. "There is good evidence that exercise may play an important part in some cancers such as colon and breast," Dr. Bernard Levin, head of the American Society of Clinical Oncology's (ASCO) Cancer Prevention Committee, told Reuters Health. Results of the survey, a joint effort by ASCO and the Cancer Research and Prevention Foundation, were released at ASCO's annual meeting. Only one-third of respondents felt that maintaining a healthy weight was important in cancer prevention. On the contrary, maintaining a healthy weight is one of the best ways to reduce the risk of a number of cancers, including those of the colon, pancreas and breast, according to Levin. Recent research suggests that as many as one-third of all cancers may be related to obesity.

But Levin was particularly disturbed by the survey findings on sunscreen. Only about one-third of respondents said they always put on sunblock before going to the beach or pool. "We know that skin cancer is one of the most preventable cancers and, in some parts of the country, one of the fastest growing," Levin said.

Thirty-four percent of those surveyed strongly agreed that they are at increased risk of developing cancer if a family member has had cancer, and nearly two-thirds said they or an immediate family member has had cancer.

On the vitamin front, nearly 30 percent felt strongly that taking vitamins or herbal supplements will reduce their risk of getting cancer. "But, in fact, there are no scientific studies on herbal supplements that show they have any effect on reducing cancer risk," Levin said. "In general, the best way to get these nutrients is from their natural source, which is in the diet."

When it comes to tobacco, the vast majority of respondents knew that tobacco plays a role in causing cancer. However, 39 percent of those who said they have smoked continue to do so. This shows a clear "discrepancy between belief and practice," Levin said. Overall, according to Levin, the survey shows that "Americans need clear information on what they can do to reduce their risk of cancer."

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The Best Offense Against Cancer-(ET-03/06/2003)

Oncologists recognize that rather than trying to kill cancer after it has started to spread through the body -- the situation for more than 50% of patients at diagnosis -- it would be far better to stop the disease from occurring in the first place, or at least detect it earlier. That's why attendees at the American Society of Clinical Oncology [ASCO] meeting were eager to hear about several new studies that addressed these issues. The most intriguing: data showing that statins, the popular cholesterol-lowering drugs, may also prevent cancer, and that magnetic resonance imaging [MRI] scans are far more effective than mammograms in identifying early stage breast cancer.

The statin study is part of a growing body of research into drugs that may prevent cancer from developing in high-risk patients. In a Dutch study, Matthijs Graaf and colleagues at the University of Amsterdam compared the medical records of 3,219 heart-disease patients taking statins with 16,976 non-statin users. After accounting for all other drugs and other health issues, they found that statin use was associated with a 20% reduction in cancer risk. The relationship was most compelling for patients who had taken statins for more than four years. And the correlation fell off once statin use was stopped for more than six months. The drugs seemed to reduce the risk of all cancers, but the declines were greatest in prostate and kidney cancer.

Graf said that about 80% of the patients studied were taking Zocar, made by Merck, but several other statin drugs were also used. He speculated that the protective benefit may stem from the fact that statins inhibit an enzyme in the liver that may be an important pathway in the formation of cancer.

A second European study, from researchers at the University of Bonn in Germany, found that MRIs are significantly more sensitive than mammography for diagnosing breast cancer in women with a genetic risk of the disease. Women who inherited the so-called BRCA gene mutation have an 80% to 90% risk of developing breast cancer, often while still in their 30s. Dr. Christiane Kuhl and her colleagues examined 462 of these high risk women over a five year period, screening them each year with a mammography, ultrasound, and MRIs. The MRI was by far the most sensitive screening technology, picking out 96.1% of early stage tumors, compared with 42.8% for mammograms and 47% for ultrasound. The MRI scans were also associated with the lowest rate of false positives.

The German study was backed up with a smaller study of 54 women with BRCA mutations conducted by doctors at Memorial Sloan-Kettering Cancer Center in New York. However, Dr. Mark Robson of Sloan-Kettering said the MRI scans, while 100% accurate in detecting small tumors, also resulted in a high number of false positives. Out of 12 biopsies done after a worrisome scan, only two turned up cancerous tissue. Robson did not recommend widespread MRIs because of this lack of specificity. Also, the procedure is extremely expensive, costing about $2000 per scan, vs. $300 to $400 for a mammogram. Kuhl of the University of Bonn was slightly less cautious, but warned that MRI scans are most effective when administered by highly skilled practitioners with considerable experience with the technology.

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Personality Doesn't Influence Cancer Risk: Report-(Reuters Health-03/06/2003)

Despite the ancients' belief that melancholy can lead to cancer, new research suggests that your personality has no influence on whether or not you develop the disease. Japanese researchers discovered that people who fit certain personality types -- as in people who were especially extraverted, neurotic, tough-minded or prone to lying -- were no more likely than others to develop cancer over a seven year period. Study author Dr. Yoshitaka Tsubono of Tohoku University told Reuters Health that these findings show that people who want to reduce their risk of cancer should focus on factors that have shown to have a significant impact on the disease: namely smoking, heavy drinking, obesity and lack of exercise. "Although further studies are needed, our results indicate that we do not have to worry about changing our personality to prevent cancer," Tsubono said.

The researcher noted that theories regarding personality's effect on the risk of cancer date back to 200 AD, but recent reports have shown mixed results, and suggested that the potential influence personality has on cancer may not be so straightforward. "Although modern studies have been conducted since the 1960s, there have been controversies as to whether personality causes cancer, or cancer causes change in personality," Tsubono said. To investigate the question themselves, the researchers asked 30,277 residents in Japan to complete personality tests and describe their health behaviors, then followed those residents for seven years to determine who developed cancer. Almost 700 people were already diagnosed with cancer when the study began, and another 986 developed the disease during the following seven years. The researchers focused on certain personality traits: extraversion, neuroticism and psychoticism -- described as liveliness, emotional instability and coldness, respectively -- as well as a trait marked by lying and social conformity.Overall, people who had strong tendencies toward each of the four personality types were no more likely than others to develop any type of cancer, nor did they show higher risks for individual cancers -- namely, cancer of the stomach, lung, colorectum and breast.

The lack of relationship between cancer risk and personality remained even when the authors removed the influence of other factors, such as smoking, body weight and family history of cancer. People who had a tendency toward neuroticism were more likely to have already been diagnosed with cancer before the study began, and more likely to develop cancer during the first three years of the study. However, the increased risk of cancer among overly neurotic people eventually disappeared. Neurotic individuals are more prone to worrying and anxiety. Writing in the Journal of the National Cancer Institute, the authors suggest that people's neuroticism may be a result of a cancer diagnosis, rather than the cause. Early cancer may have caused some people to become more neurotic, they note, and people whose cancer was diagnosed during the first years of the study may have already had symptoms of the disease when the study began. These early symptoms, even without a diagnosis, could also have caused people to become more neurotic over time, the authors write.

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Data Demonstrate the Predictive Role of Bone Marker in Identifying Patients at High Risk of Cancer-Related Bone Complications-(ET-02/06/2003)

Data show that the bone marker N-telopeptide (Ntx) may predict the clinical outcome of patients with bone complications that stem from a variety of different cancers, according to a study presented at the American Society of Clinical Oncology (ASCO) meeting in Chicago, Illinois, USA. These results demonstrate the potential role the bone marker may have in providing an early warning of potential skeletal complications and need for treatment of bone metastases, providing physicians a powerful tool in patient management. The analysis included data from three major clinical trials evaluating zoledronic acid in more than 3,000 patients who suffer from a broad range of tumor types, such as breast, prostate, lung and other solid tumors and multiple myeloma. The data from these studies are the most extensive available and present an unprecedented opportunity to analyze the predictive roles of bone markers for subsequent skeletal complications.

Research indicates that many patients with advanced cancers will develop bone metastasis, the spread of cancerous cells from the original tumor to bones. Often, bone is the only site of metastasis in these patients. Complications resulting from bone metastases include, among others, bone pain, pathologic fractures, a need for radiation or surgery to bone, spinal cord compression, and change of antineoplastic therapy to treat bone pain and hypercalcaemia. "Bone metastases and their complications can be severely debilitating for advanced cancer patients with a highly negative impact on quality of life," said Dr. Janet Brown, Cancer Research Centre, University of Sheffield, U.K. "Based on our data, it may now be appropriate to consider routine measurement of Ntx in the management of patients with metastatic bone disease with the aim of normalizing the Ntx value with bisphosphonates."

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