BLOOD CANCER

Analysis of gene expression in lymphoid cells can determine lymphoma cancer-(Yahoo News-18/08/2004)

Analyzing the expression levels of the gene CDK9 (cyclin dependent kinase) and its attached molecule CYCLIN T1 in lymphoid cells in a sample of blood can accurately pinpoint lymphoma, according to researchers at Temple University's Sbarro Institute for Cancer Research and Molecular Medicine and the Department of Human Pathology and Oncology at the University of Siena in Italy. Their study, "CDK9/CYCLIN T1 expression during normal lymphoid differentiation and malignant transformation," appears in the Journal of Pathology (Volume 203, Issue 4).

Lymphomas are generally difficult to diagnose since no single test currently exists to sufficiently establish their presence. Clinical practice often revolves around a pathologist looking for changes in normal lymph node architecture and cell characteristics through a series of tests, such as blood tests, x-rays, computerized tomography (CT) scans, magnetic resonance imaging (MRI) and bone marrow biopsy. "There are many types and subtypes of lymphoma, some of which are easy to detect, but many that are very difficult to identify," says Antonio Giordano, M.D., Ph.D., director of the Sbarro Institute at Temple and one of the study's principal investigators.

The researchers found that by taking a sample of blood and doing immunohistochemical analysis for the expression of CDK9 and CYCLIN T1, they were able to accurately pinpoint the type of lymphoma--Hodgkins or non-Hodgkins--as well as its stage of advancement. Non-Hodgkins lymphoma is the sixth-most common cancer in the United States. "Basically, this new method is a very powerful tool in determining the presence of cancer by analyzing these two molecules in the lymphoid tissue," explains Giordano, an internationally recognized researcher in the genetics of cancer and gene therapy. "The change of levels of CDK9 and CYCLIN T1 in lymphoid cells shows a correlation with activity of the cancer. The higher the expression of the gene and the attached molecule in the blood sample, the more likely for lymphoid cancer."

CDK9 was originally isolated by Giordano, who at the time was a researcher in Temple's Fels Cancer Institute, and his team in 1992. A member of a family of kinases, CDK9 was originally referred to as PITALRE, the name of the amino acid sequence that is similar in all members of this kinase family. "We were screening a human DNA library in order to look for members of this family, and we found CDK9, a gene that encodes for a protein that has the size of 43 kilodaltons," says Giordano, who is also co-director of the Center for Biotechnology in Temple's College of Science and Technology. 

Over the next 10 years, CDK9 would prove to be a "multi-functional" gene, playing many different roles. According to Giordano, among the many functions of CDK9 that have been discovered, one of the most interesting is the role of this kinase in cellular differentiation, particularly muscle differentiation. "In practical terms, when we overexpress this protein, we are able to promote myogenic differentiation by enhancing the myoD function," says Giordano, who also discovered the tumor suppressing gene Rb2/p130. "Our studies have demonstrated that in human tissue, CDK9 is a very important player in specialized tissue, as we see in this study with lymphoid tissue."

 [Back]

Environment may be linked to rising leukaemia-(Reuters-06/09/2004)

Pesticides or chemicals in the environment may be behind the steady rise in cases of childhood leukaemia, which have increased five-fold since the early 1900s, scientists said on Monday. Fewer children actually die from the blood cancer than 40-50 years ago but cases have increased about one percent per year in the last half century. "It represents a five-fold increase," Professor Michel Coleman of the London School of Hygiene and Tropical Medicine told a conference delving into the causes of the increase.

From about 10 cases per million population in England and Wales in 1911-1915, cases rose to about 46 per million at the end of the century. "The evidence suggests a steady increase in the occurrence of leukaemia in this country and in others," said Coleman.

Leukaemia is the most common childhood cancer, accounting for nearly one-third of all cases. Most of the rise is in children aged 1 to 4. Boys have about a 10 percent higher risk of developing the disease, according to Coleman. Professor Denis Henshaw of the University of Bristol in south-western England and chairman of the conference, said a possible cause could be environmental agents or chemicals that were not around 50 years ago. Children are thought to be predisposed to the illness at birth by something that occurs in the womb but they do not develop it unless it is triggered by causes as yet unknown. Ionising radiation, electromagnetic fields, viruses, infections and chemicals and pesticides are thought to be possible triggers.

Professor Alan Preece, also from the University of Bristol, presented research showing the unborn child is particularly sensitive to the effects of exposure to such agents. In laboratory and animal studies, Preece found levels of such compounds were higher in the foetus than in the placenta or the mother. "The environmental agents cross the placenta and accumulate in certain foetal organs, varying according to the nature of the agent," Preece said. "The exact levels are as yet unknown but we know that childhood leukaemia is initiated in utero and this could well be a factor in the initiation."

[Back]

Multiple Myeloma Research Consortium Launched as New Model to Accelerate Drug Development for Blood Cancer- (PRNewswire- 17/08/2004)

Consortium (MMRC), a first-of-its kind non-profit organization that integrates four leading cancer research institutions, was announced today.  The MMRC is the only consortium to join academic institutions both through membership agreements and customized IT systems. MMRC-affiliated institutions will focus on the identification and validation of molecular targets for multiple myeloma, the discovery of drugs against these targets and expediting the early phase trials of these drugs.  The ultimate goal of the new Consortium is to rapidly advance the drug development process and find a cure for multiple myeloma.

Founded by Multiple Myeloma Research Foundation (MMRF) President Kathy Giusti, this innovative model, which was funded by a grant from the MMRF and developed in collaboration with PricewaterhouseCoopers, will provide these institutions with the ability to share their expertise and research data to accelerate the testing of new, lifesaving therapies and eliminate much of the duplication that is now prevalent in the drug discovery process. 

MMRC Member Institutions include Dana-Farber Cancer Institute, H. Lee Moffitt Cancer Center & Research Institute, Mayo Clinic and University Health Network  (Princess Margaret Hospital). These institutions were selected based on their National Institutes of Health grant awards, number of peer-reviewed publications, clinical expertise, and a collaborative approach to science.     Multiple myeloma, a cancer of the plasma cell, is an incurable but treatable disease. There are approximately 50,000 people in the United States living with multiple myeloma and each year an estimated 11,070 people die from the disease.  Multiple myeloma is the second most prevalent blood cancer after non-Hodgkin's lymphoma. "Despite recent successes in treating some myeloma patients, myeloma remains an incurable disease. With a five-year survival rate of only 32%, new therapies are urgently needed," explains Kathy Giusti, President of the MMRC, who is also a multiple myeloma patient. "We recognized that there was a major disconnect in the research and drug discovery process because institutions are not easily able to quickly and accurately share necessary data on corresponding projects. The MMRC will allow them to unite their research to speed target identification and drug development." 

The MMRC sets itself apart with the creation of the MMRC Tissue Bank, which will serve as an invaluable resource of tissue and corresponding clinical and genomic data necessary develop new, targeted therapies. All samples maintained within the Tissue Bank will be collected, analyzed, and stored in adherence with government-regulated Good Laboratory Practice standards.   This centralized repository will enable scientists from academia and industry to identify and validate molecular targets for multiple myeloma and drugs active against these targets, as well as to more quickly determine a patient's response to existing drug therapies. "By having one source of genomic data and tissue samples that have been uniformly standardized, as well as an integrated validation and multi-center clinical trials system, this will reduce the drug development process by months and possibly years. This should help us to bring more specific and hopefully more effective drug treatments to patients more rapidly," explains Kenneth Anderson M.D., chairman of the MMRC Leadership Team.

Complementing the MMRC Tissue Bank is the MMRC Data Bank, a state-of-the-art system that integrates laboratory and clinical trial data into one common interface, allowing researchers to effectively conduct early phase trials with a focus on correlative science.  MMRC Member Institutions will conduct research in three multi-site research cores: Genomics, Validation and Clinical Trials that will remain highly integrated.  The customized infrastructures at the MMRC were designed by IBM Life Sciences and First Genetic Trust to ensure the seamless transfer of tissue and data across multiple institutions.

 [Back]

'Infertile' cancer survivor pregnant-(Yahoo News-20/06/2004)

A WOMAN made infertile by cancer treatment is expecting a baby after undergoing an ovarian tissue transplant, it was revealed yesterday. The breakthrough opens the way to motherhood for thousands of women whose ovaries have been destroyed by cancer treatment. But there are also major ethical implications, because potentially the technique could be used to beat the menopause. A career woman nearing the end of her reproductive life could, for instance, choose to have ovarian tissue frozen and restored to her at a later date. She would then be capable of getting pregnant after the start of the menopause.

News of the breakthrough came yesterday at the annual meeting of the European Society of Human Reproduction and Embryology in Berlin. The 32-year-old patient is the first in the world to become pregnant as a result of the experimental procedure. Tissue samples from her ovaries were taken in 1997 and frozen before she underwent chemotherapy and radiotherapy for advanced lymph cancer. After the treatment, the ovarian tissue was thawed and implanted back into her. In January, 11 months after the transplantation, doctors discovered she was pregnant. Now the woman is not only free from Hodgkin’s lymphoma but also expecting a baby girl in October.

Support groups hailed the achievement by a team in Belgium as a landmark in fertility treatment. Experts were discussing new developments in ovarian transplants when it emerged that the woman treated by Professor Jacques Donnez, at the Catholic University of Louvain in Brussels, was pregnant. Prof Donnez heads one of three or four teams in the world conducting ground- breaking research in this area. He said in an interview with a Belgian radio station: "She is pregnant. She lives a life which she could not hope she would be able to live in 1997. She knew that she was going to be post-menopausal, and now she is expecting a child, her own. "It’s her child genetically, growing from her tissue, and she fell pregnant completely naturally, through having sex. She is very happy."

One of the leading pioneers in the field is Dr Kutluk Oktay, from Cornell University in New York, who carried out a similar procedure on a woman treated for cancer. In March he announced that her attempted pregnancy had failed. He said: "If they prove that this did not come from a natural recovery of ovarian function then it is a landmark. The field is progressing rapidly. In the next few years you’re going to see lots more pregnancies. Many cancer patients see this as the only bright spot in their dealings with their disease. They see it as a bridge between them and their future. It helps them cope with cancer and have a much more positive attitude to what they’re going through."

Dr Yding Andersen, from the University Hospital of Copenhagen, who is waiting to see if an ovarian transplant patient he has treated becomes pregnant, said: "It’s definitely a breakthrough and it has huge implications for a lot of women around the world. If this will lead to the birth of a child it is very, very, fantastic."
His patient, who was also treated for Hodgkin’s lymphoma, produced eggs from an ovarian transplant which were used to make an embryo in-vitro. The embryo has now been transferred to her womb.

A spokeswoman for Infertility Network UK said: "We would absolutely welcome this breakthrough and it seems tremendously exciting. It will give new hope to women who have undergone treatment for cancer and would otherwise be facing a lifetime of childlessness."

[Back]

ALL survivors bear genetic damage from life-saving chemotherapy- (Yahoo News-01/07/2004)

Children who undergo chemotherapy and survive acute lymphocytic leukemia (ALL) endure a 200-fold increase in the frequency of somatic mutations in their DNA, researchers from the University of Vermont Medical School reported in the July 1 issue of the journal Cancer Research. The alterations in the children's gene sequence remain embedded within their chromosomes and may pose elevated risk for development of second malignancies and other diseases later in life, cautioned Barry A. Finette, M.D., Ph.D., associate professor of pediatrics at the University of Vermont. "The treatments that are used to help children defeat this disease are keeping a very large percentage of them alive," Finette said. "Pediatricians are continually monitoring these children as they live beyond five, ten, and more recently, 15 years after their ALL is in remission. We now need to be proactive about studying any long term genetic ramifications that these children may face due to the treatment therapy they endured during their bout with cancer."

Finette noted that children who are cured of ALL after chemotherapy have a 5-20 times greater risk of developing secondary malignant neoplasm's as well as other complications. Subsequent illnesses may be associated with increased changes in the patient's genes resulting from their treatments during ALL therapy. Finette and his team of scientists examined the frequencies of alterations found within a marker gene in the blood cells of ALL patients at four intervals, between the time they were diagnosed until after they had completed their treatments. By examining the number of T cells in the patients' blood that contained mutations in the HPRT reporter gene, the researchers estimated how frequently chemotherapy altered the DNA sequence within that specific marker gene.

The research showed that at the time of diagnosis, the blood of patients contained an average of 1.4 cells with HPRT mutations out of every million T cells, Finette said. The treatment for ALL consists of a three-phase regimen, including induction, consolidation and maintenance. By the time the patients completed their consolidation phase of treatment, an average of 52 T cells per million cells contained HPRT mutations. By the final stage of treatment, an average of 93 of every million T cells had mutations in HPRT. After treatment was stopped, an average of 271 of every million T cells contained HPRT mutations, more than a 200-fold increase.

The study included 45 children with ALL who averaged 5.5 years of age at time of diagnosis. The number of HPRT mutations found in the patients at the time of diagnosis did not differ from healthy children of the same age, the researchers reported. The increase in genetic mutations seen in the ALL patients accumulated over the course of their treatments. "The mutations that arise during treatment for ALL remained elevated after completion of therapy," Finette noted. But in the absence of the mutagenic chemotherapy, the rate of further genetic damage subsided. The post-treatment rate of HRPT mutations in the ALL survivors paralleled the number of new gene alterations observed in healthy children of similar age.

The chemical therapeutics administered to the patients, however, are powerful, and while they are designed to keep cancer cells from proliferating and to induce cancer cell death, normal cells can also be affected. "The therapies used to assist these children overcome ALL have the potential to cause genetic damage to many different cell populations in their rapidly growing bodies," Finette said. "Because they have larger numbers of replicating cell populations during their growth and development stages than adults have, they are more susceptible than adults to effects of the chemotherapies genotoxicity." ALL is the most common pediatric malignancy, but many ALL patients respond well to chemotherapeutic interventions. Since the 1960s, the five-year survival rate for children with ALL has increased to almost 80 percent. Patient remission and long-term survival is credited to the development of national standardized chemotherapeutic treatment protocols. More than 70 percent of ALL children less than 20 years of age, and 85 percent of children less than 15 years old participate in the standardized ALL chemotherapy treatment regimes.

"Because of the effectiveness of the treatment employed today, we are able to give many more children a chance for a long life without cancer," Finette said. "Our studies are aimed at enabling us to better understand further challenges that we may face in keeping these patients healthy as they get 10, 15 or more years out from overcoming ALL."

[Back]

Freezing Cord Blood and Stem Cells - Should You or Shouldn't You?-(Business Wire-03/06/2004)

The mere mention of stem cell research can stimulate a heated discussion among the medical and non-medical crowd alike. However, there is a non-controversial method of collecting stem cells, via placental and umbilical cord blood from newborns. There are even several companies advocating the saving and freezing of those stem cells for future family use, but the question for expectant parents remains, should they do it? When does it make sense to save and store cord blood and at what expense?

"I am asked all the time if expectant parents should save and freeze their baby's cord blood. My answer is yes -- and no. Perhaps Yes, in the rare case where there is a family history of a specific illness which could be treated with cord blood stem cells, or if a cord blood transplant could help a sibling suffering from specific types of cancer. However, there are many instances in which cord blood couldn't or shouldn't be used, even in those cases involving the infant himself. The odds that the average baby will ever use its banked cord blood have been estimated at 4 in 10000 or .04%," states Dr. Curt Civin, Samuelson Professor of Oncology and Pediatrics at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University School of Medicine and medical advisory board member of the Sidney Kimmel Foundation for Cancer Research.

Dr. Civin adds that the money spent on freezing and storing cord blood for the average family, which can range from $1,200 - $1,800 for the first year and $100 every year thereafter, might be better put into a savings bond for college.

"On the other hand, I often tell expectant parents that harvesting their baby's cord blood could actually save the life of another child suffering from leukemia or other bone marrow illness and therefore donating that blood could have an immediate and positive impact on the life of an unrelated child," states Dr. Civin.

Public banks for the storage of cord blood have increased dramatically in recent years thanks in large part to the American Red Cross. And, according to the National Marrow Donor Program, there are more than 80 locations across the country from Alabama to Washington.

While only a few thousand cord blood transplants have been performed since 1989, the list of diseases that can be treated through this method grows each day thanks to dedicated scientists around the globe. Currently research with cord blood stem cells is going on involving AIDS, Alzheimer's, diabetes, heart disease, liver disease, MS, Parkinson's, spinal cord injury and stroke, although it will likely be many years before these basic research result in clinical treatments.

Currently many children and even some adults could benefit from donated cord blood. So if you are looking to put your baby's cord blood to good use, visit www.marrow.org and find a hospital near you. To weigh in on this issue and see what others are thinking, visit www.kimmel.org and click on the survey button on the right hand side of the screen. 

[Back]

New studies show promise of gene analysis in fighting cancer-(Yahoo News-19/04/2004)

Looking deep inside the genes of malignant cells, two teams of leukemia researchers have uncovered new ways to help identify the severity of a patient's cancer, the best treatments and how long a patient might live. The studies, carried out by teams at Stanford University and in Europe, rely on a detailed analysis of cancer genes to understand how a malignancy is likely to progress and how best to fight it. While this type of gene analysis isn't being used on leukemia patients yet, doctors say it probably will play an important role in treating the most common form of adult leukemia. More broadly, the findings, published in New England Journal of Medicine, mark another important step for the use of gene analysis in fighting cancer. This field of research is shedding light on the disease's basic wiring, uncovering whether some cancer cells are more lethal from the start. Such genetic predictors have previously been teased out of lymph, breast and prostate cancers. By screening gene activity at a very detailed level, researchers have found they can sometimes look at different tumors from the same type of cancer and tell how each will progress. That information may help doctors choose the best care for a patient, or even lead to new treatments. But for patients whose cancer genes look ominous, such advances might only mean more worry.

The new leukemia studies "are very significant advances," said Dr. Marshall Lichtman, executive vice president for research and medical programs for the Leukemia and Lymphoma Society. "But it's still early in the game. It's going to take some real doing to use this to tailor therapy." In one of the studies, led by Stanford scientist Dr. Jonathan Pollack, researchers isolated a group of 133 genes from cancer cells gathered from 116 adults with acute myeloid leukemia. This cancer of the blood and bone marrow is diagnosed in more than 10,000 Americans each year, according to the American Cancer Society. Among adults, it has the lowest survival rate of any of the major forms of leukemia, with about 20 percent of patients alive five years after diagnosis.

Pollack's team started with genes from patients with "intermediate-risk" cancer. Doctors already use broader genetic tests to analyze a patient's leukemia, but in most intermediate risk cases, those screenings have failed to show the cancer's severity. When the researchers examined the group of 133 cancer genes at a molecular level, they realized the once-indistinguishable cancers fell into two different activity patterns. Those activity patterns matched how long the intermediate-risk patients lived - overall a little less than a year for the group whose cancer genes indicated a poor outcome, and a little less than two years when the genes indicated a better outcome. A similar pattern emerged for all 116 patients. Those with more ominous cancer genes lived a little less than a year overall, while those with more promising genes often lived between three to four years, Pollack said.

Acute myeloid leukemia is often treated with chemotherapy, sometimes followed by a bone marrow transplant. The transplant, which is risky, is usually reserved for more dangerous cancers, and such genetic analysis may make it easier for doctors to know when to use it. "What looks like one disease may really be two," Pollack said. "This can really improve our understanding, and help choose the best therapies." For patients, that kind of discovery carries a heavy dose of promise - or pain. "I wouldn't want to hear, `Sorry, given the genetics, there's not much we can do for you,'" said Joanne Arneal, 40, a leukemia survivor who lives in the East Bay and counsels newly diagnosed patients. "If you're on the losing end of that news, you still have to find a way to keep going on." Diagnosed with acute myeloid leukemia when she was 25, Arneal quickly realized what helped her - and what didn't - as she fought her leukemia into remission. Any glimpse of the future gleaned from gene scans need to be handled with care, she said. "I remember asking my oncologist once `What are my chances?' and he said `About 25 percent,"" she said. "All I could think was `Why did I ask that question?' Half the battle is the mental battle."

Pollack said the aim of the studies, also conducted at labs in Germany and the Netherlands, is to give patients more hope, not less. He and other researchers are confirming the study results, and if that goes well, a full-scale clinical trial using the gene scans in patient treatment could begin in a year or two, he said. "This will help patient care in the not-too-distant future," said Pollack.

[Back]

Stem Cells Help Attack Cancer in Mice-(AACR Meeting)

Stem cells, immature cells already showing promise as tools to regenerate and replace damaged tissue, may also help target and destroy cancer, U.S. scientists said on Monday. Tests in mice showed the cells could deliver powerful cancer-killing proteins, destroying tumors while leaving healthy cells untouched. Dr. Michael Andreeff and colleagues at the University of Texas M. D. Anderson Cancer Center in Houston used cells taken from bone marrow. These immature cells, known as mesenchymal stem cells, usually give rise to muscle and other tissues. The researchers genetically engineered these cells to carry interferon alpha, an immune system protein that can help kill cancer cells, or a cancer-destroying virus. In mice these cells slowed several kinds of leukemia, attacked melanoma -- skin cancer and breast cancer cells -- that had spread to the lung, and tackled brain tumors. The approach cured 70 percent of mice implanted with one kind of human ovarian cancer, the researchers told a meeting of the American Association of Cancer Research in Orlando, Florida. "This drug delivery system is attracted to cancers, both primary and metastatic, and anti-tumor effects are observed when the cells integrate into the tumor micro-environment," Andreeff said in a statement. "The most important discovery here is that these cells are capable of migrating from the bone marrow or blood circulation selectively into tumors and produce anti-tumor agents only at the sites of these tumors and their metastasis." Andreeff said tumors attract mesenchymal stem cells by sending out signals similar to those sent by damaged tissue

[Back]

Experts: Research Needed Into Rising Teen Cancers-(Reuters-01/03/2004)

Cancer in teenagers and young adults has risen to become the most common cause of natural death for their age, but not enough research is being done into its causes or treatment, health experts said. Cancer among 13-24 year olds is still rare, with about 1,500 new cases diagnosed each year in Britain. But while survival rates for children and adults with the disease have improved in recent decades, they have remained unchanged for adolescents and young adults. "We've orphaned this particular age group," Professor Archie Bleyer, of the University of Texas MD Anderson Cancer Center in Houston, told the Third International Conference on Adolescent Cancer. "Young people and older adolescents have been left behind."Bleyer and other cancer experts said teenagers have fallen into a medical gap. Although they develop specific types of cancer and have different medical and psychological needs, they are either treated as children or adults. Little is known about the causes or risk factors of teenage cancers, yet few young people are involved in clinical trials to discover underlying reasons why they develop the disease or the best ways to treat it. "There is a great need for high-quality research," said Charles Stiller, of the University of Oxford.

In one of the largest studies done into teenage and young adult cancer involving 21 years of data, Professor Jill Birch of the University of Manchester in England, said cases in Britain have risen from 15.4 to 19.8 per 100,000 between 1979 and 2000 -- an average increase of 1.2 percent per year. Leukemia was most common in 13 and 14-year-olds, followed by lymphoma and brain tumors. But by 15 and above, lymphoma accounted for the great number of cases. "The early age of onset and lack of opportunity for chronic exposure to environmental factors suggests that genetic susceptibility may be important," said Birch. But she added that genetic mutations probably only account for a small number of cases. "What is more likely is that a cancer develops as a result of exposure to a risk factor in a genetically susceptible individual," she said. Early exposure to viruses, passive smoking and lifestyle changes, particularly increased sun exposure, may also play a part. Rates of melanoma, the most serious type of skin cancer, have almost doubled over 21 years in the 20-24 age group in Britain and it now accounts for one in 10 of all cancers. "Worldwide, we need a new discipline in adolescent and young adult oncology," said Bleyer. "Until we devote resources specially to this age group, there will be little progress," he added

[Back]

Beating Multiple Myeloma-(HealthDayNews-24/02/2004)

A discovery by U.S. researchers may help lead to new ways to treat multiple myeloma, an incurable cancer of immune cells called plasma cells found in the blood and in bone marrow. The study, in the February issue of Cancer Cell, identified a frequent and common abnormal cellular event that occurs in about half of all cases of multiple myeloma. This finding provides scientists with a potential treatment target. In this U.S. National Cancer Institute-led study, scientists focused on a cancer-causing gene called c-maf. They found c-maf was present in about half of all myeloma cases but was absent from normal plasma cells. The study also found c-maf increases production of factors that directly promote tumor cell growth and the factors that promote tumor cell growth indirectly by increasing adhesion of pathological tumor cells to other types of cells within the bone marrow.

The scientists say they also determined that inhibiting c-maf function in myeloma cells blocked tumor formation in mice. "Our results indicate that overproduction of c-maf is one of the most common abnormal events associated with myeloma. Further, our finding that inhibition of c-maf blocks myeloma proliferation and tumor formation makes c-maf an intriguing and exciting novel target for future therapies," research team leader Dr. Louis M. Staudt, of the National Cancer Institute, says in a prepared statement.

[Back]

Aspirin May Lower Risk of Hodgkin's-(ET-18/02/2004)

Scientists have found a hint that regular aspirin use might lower the risk of Hodgkin's disease, but more research is needed to prove it. Even if the link is real, Hodgkin's is too rare a cancer to recommend aspirin as a preventive, scientists caution, since the pills can have side effects. Instead, the research may point toward better understanding of how this cancer forms, important for future work on treatments. Millions of Americans already take low-dose aspirin to help prevent heart attacks, and studies suggest it also may modestly lower the risk of a few cancers, most notably colon cancer. Scientists at the Harvard School of Public Health uncovered aspirin's possible connection with Hodgkin's - a lymph system cancer diagnosed in 7,600 Americans a year - while studying what role a certain virus plays in the malignancy.

To hunt risk factors, they matched 565 Hodgkin's patients with people of similar age and demographics who didn't have the cancer. Those who regularly used aspirin - the equivalent of two or more regular-strength tablets a week for five years - had a 40 percent lower risk of Hodgkin's, researchers reported in the Journal of the National Cancer Institute. Hodgkin's disease is linked to inflammation. Aspirin not only calms inflammation, but it is thought to inactivate a protein, called a transcription factor, important for Hodgkin's cells to survive, said epidemiologist Ellen Chang, the study's lead author. Other painkillers don't affect that protein, and the study found no benefit from other anti-inflammatory painkillers, such as ibuprofen. However, acetaminophen is a different type of painkiller, and the study found risk of Hodgkin's was 70 percent higher among regular acetaminophen users. The researchers caution people not to be frightened by the acetaminophen finding, because they are suspicious that it could be wrong. The Hodgkin's patients may have used acetaminophen because of early symptoms of their cancer, thus confusing the research, Chang said. "There's no clear biologic reason why acetaminophen would be associated with higher Hodgkin's disease risk," said Chang, now with Sweden's Karolinska Institute. But "it makes sense that aspirin could be associated with lower Hodgkin's risk" because aspirin has the unique transcription-factor inactivation, she said.

The study raises an interesting hypothesis about aspirin, but just how strong a role the transcription factor plays is contentious, said Dr. Ernest Hawk of the National Cancer Institute. "Even if it is confirmed, these results do not mean that anybody should take aspirin to prevent cancer," said American Cancer Society epidemiologist Eric Jacobs. Aspirin can have serious side effects in some patients, including bleeding and digestive ulcers. Both cancer specialists minimized the acetaminophen finding

[Back]