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