|
|
              
 |
Abstracts by Bruce Shriver and Tom Swartz
Spontaneous Regression of Advanced Cancer in Mice For the last few years, scientists at the Wake Forest University School of Medicine Department of Pathology have been engaged in a project that revolves around a unique mouse serendipitously discovered in 1999, known as the SR/CR Mouse. The original mouse of this type was part of an experiment in which mouse cancer cells were being transplanted into the abdominal cavity of other mice to produce cancer. This particular mouse, a member of a highly inbred strain of mice, did not develop the expected tumor, even though it was injected with a large number of tumor cells. When it was injected many times more with these cancer cells, it still failed to develop a tumor. Since the cancer cells used for the injections were from a type of sarcoma, this result was seen as highly unusual. To determine if this resistance was genetic, this mouse was bred to other normal mice, and it was shown that this resistance to cancer was inherited. Also, the pattern of inheritance showed that it probably was caused by a single mutation in a single gene and was “dominant” (it only required one copy to work).
After the initial experiments, breeding studies allowed this gene mutation to be passed on to a large number of offspring from the original mouse through multiple generations. In addition to the original mouse strain, the cancer resistance could also be bred into other inbred strains of mice with different genetic backgrounds. Further studies will allow the precise mutation in the gene involved to be identified, although this is a highly complex process. An important question in studying these mice was whether the resistance to cancer only worked against the type of sarcoma injected, or it would work against other types of cancer. Using several different mouse cancer types, such as leukemia, lymphoma, liver cancer, and lung cancer, it was shown that the SR/CR mouse was resistant to all of them.
Because the initial experiments used tumor cells that were transplanted by injection into the abdominal cavity of mice, the injected cells could be recovered at a later time and examined. When this was done, it was found that injected cancer cells were killed within the first day after they were injected. In addition, other cells from the resistant mouse, mostly white blood cell types, were found attached to these cancer cells prior to their death forming “rosettes” around the tumor cell.
The white blood cell types found in these rosettes included polymorphonuclear leukocytes (a common white blood cell involved in killing bacteria in infections), monocytes (a common white blood cell type that can also crawl into tissues where it is called a macrophage) and a special type of immune cell called a natural killer cell (NK cell). All of these cells are part of what is referred to as the “innate immune system,” cells that are active against many foreign organisms, such as bacteria, viruses and fungi, without prior immunization. Surprisingly, very few of another type of white blood cell -- lymphocytes (T cells or B cells) were found. Such cells are normally part of the rejection of foreign cells by the immune system, and are frequently involved in more familiar cell rejection events, such as those seen in the rejection of poorly-matched tissues and organs (kidney, bone marrow or skin transplants). Clearly, something other than normal tissue transplant rejection was happening in these cancer-resistant mice.
To further rule out that the cancer cells were killed not because they were foreign, a cross-breeding experiment was done, in which one mouse with the SR/CR cancer resistance trait was bred with a mouse that was genetically deficient in T cell function (a so-called “nude” mouse). Several generations later, the offspring from that mating including some mice that had the SR/CR cancer resistance trait, yet were still defective in normal organ rejection, were still cancer-resistant. This showed that the cancer resistance mechanism operates even in a mouse that cannot reject mismatched organ transplants. Thus the resistance mechanism doesn't use T-cells.
Another important finding with these mice is that the cancer resistance seems to be age dependent. The original cancer resistance occurred in mice that were six weeks old (just post-adolescent for a mouse). When testing for cancer resistance was delayed until 5 months of age, the mice that had inherited the resistance gene began to grow tumors, just as normal mice do. However, when the tumors reached a detectable size at 2-3 weeks, many of these mice showed a sudden decrease in tumor size in a day or two, followed by disappearance of the tumor completely. In some cases, this “spontaneous regression” of cancer was quite dramatic -- a very large tumor mass disappeared overnight. What appeared to be happening in these older mice was that the cancer could grow until the anti-cancer mechanism finally “kicked” in, ultimately killing all of the cancer cells. In addition, if these spontaneously regressing mice were then re-injected with new cancer cells, they appeared now to be completely resistant. Thus, they had been primed by the prior rejection of tumor cells. In a sense, they had been vaccinated against cancer. If, however, the mice reached the age of 1 year before being exposed for the first time to cancer cells most of these mice were not cancer resistant, even though they clearly had the gene mutation (since their offspring were resistant when tested at an early age).
The spontaneous regression seen in older SR/CR mice strongly pointed to a killing mechanism of the cancer, as opposed to just a mechanism that prevented growth of the cancer. When the cancer cells of the resistant mice were recovered, the cancer cells showed rupture of the cell surface membrane, a process referred to as cytolysis. Other experiments showed that this rupture probably involves toxic proteins that are manufactured and secreted by cells of the immune system. Two of these toxic proteins (perforin and granzyme B) were found in the fluid around the cancer cells. A further important question in understanding how these mice killed cancer cells was whether the killing required live cells from the resistant mouse, or could be mediated by some floating molecule independent of intact immune cells. One way of studying this issue is to isolate cells involved in the killing mechanism from the resistant mouse and transfer them either into a normal mouse, or into a test tube with living cancer cells. In both of these tests, the cells from the resistant mice killed cancer cells, but the soluble materials did not. This strongly suggests that cells of the mouse directly attack and kill cancer cells. It also shows that resistant immune cells can be transferred to a normal mouse and, at least transiently, make that normal mouse cancer-resistant. This experiment, called 'adoptive transfer,' could be the model for a similar approach to treat cancer in people if such resistant immune cells could be generated in large numbers. Another test is to remove the immune cells from the mouse and see whether cancer could now grow. When this “immunodepletion” experiment was done, and more of the immune cells were removed, the mice gradually lost their resistance to cancer. However, when the depletion treatments were stopped, the mouse regained its immune system and the tumor regressed. This is direct evidence that the killing of cancer cells in these mice is due to cells of the immune system.
An important question in the study of the cancer resistance mechanism was whether the resistant mice were otherwise healthy. So far, studies of these mice have not shown any shortening of their life spans. There has also been no evidence that the ability to resist cancer is accompanied by some other disease problem such as autoimmune diseases. The cancer resistant mechanism in these mice is surprisingly selective, apparently only affecting cancer cells. This selective property is of great interest to scientists studying these events, since it suggests that such selectivity can actually exist and be the basis of future anti-cancer therapies.
Since the resistance seen in the SR/CR mice is an inherited trait, and appears to involve a mutation in a single gene, then the identification of the mutation and the gene which contains it can provide important clues as to how it might work. Since all of the genes of the mouse and the human have been identified from the various genome projects in the last few years, it will be possible to examine the exact mutation in the mouse and to correlate it with possible changes in similar genes in people. Mice and people have similar immune systems. It is likely that if we can understand the mechanism that is used by this mutation in mice, we will be able to apply this knowledge to identify and manipulate similar mechanisms in patients. The key to this study is the exact nature of the mutation present in these mice. Multiple studies are underway to identify this mutation and its consequences. While there are no guarantees that we can use this knowledge to treat human cancer, we can speculate on the future secrets that this information could reveal.
Bionic Arm Helps Patients Regain Use of Hands A new device called the "NESS H200" gives fresh hope to stroke victims and others who have lost hand function. A simple unit that slips over the forearm and wrist, the H200 provides neuromuscular stimulation that supports therapy and can even help restore independent function. Basically, the H200 provides electrical stimulation to the muscles of the forearm and hand. The stimulation helps the muscles directly (it actually stimulates the muscles to contract), but there may also be some carry-over in the sense of reorganizing the brain to re-enable function. We know that intact areas of the brain can take over the function of injured areas of the brain. The device allows patients to perform functions such as grabbing objects and releasing them. The major advantage of the H200 is that it is custom-fitted to the patient. The patient can actually put on and take off the device by him or herself. With the more consistent stimulation, some patients experience a return of function that was not there before. It usually takes at least a couple of weeks before there is some return of function outside the device. It does not work for everybody, but it is worth a try for many patients. There are varying degrees of improvement. Some people experience very little, while others can get up to 50% improvement in function. The H200 is not designed for permanent use, but people have used it that way because they are able to do more when they are wearing it. The same company that makes the H200 has a similar device for the legs, though it is not yet approved by the FDA. It is the same idea - it stimulates the muscles that lift up the foot and push it down. Probably even more exciting is the concept of implantable electrodes that would allow direct stimulation to the muscle. These are on the horizon. The idea is to implant "bions" in the muscle to provide direct stimulation and then "program" the muscles to contract the way we want them to. This development is years away right now.
GIST Support International – Ask the Professional GIST Support International (an all-volunteer, non-profit organization dedicated to outreach, education and support of Gastrointestinal Stromal Tumor patients, their families and friends) periodically poses questions to medical professionals. These questions are of general interest to GIST patients and their caregivers. The answers to these questions are posted on this page. Some of the recent topics include: (1) abdominal anatomy; (2) imaging GIST response to treatment; (3) the effects of Gleevec on GIST cells; (4) the grading of gastrointestinal stromal tumors; and (5) Gleevec and relapse statistics.
Long-Term Follow-Up Guidelines for Survivors of Childhood, Adolescent, and Young Adult Cancer The Children's Oncology Group has released a new, updated version of the Long-Term Follow-Up Guidelines for Survivors of Childhood, Adolescent, and Young Adult Cancer. The guidelines have been greatly expanded and reorganized to make them more user-friendly, with better graphics and references included in each section. The guidelines cover treatment agent, potential side effects, who is most at risk, and recommendations for screening for late effects. There are now a total of 42 Health Links as well, written for survivors and their families and including information on staying healthy. You can download the new guideline from the webpage that is accessed by clicking here.
Gleevec, the first oncology drug to be validated as an effective and generally well-tolerated medicine that targets a specific cause of a cancer, has marked an important five-year milestone. Gleevec is a signal transduction inhibitor. A signal transduction inhibitor interferes with the pathways that stimulate the growth of tumor cells. Gleevec was first approved five years ago in May 2001 by the US Food and Drug Administration (FDA) as a treatment for patients with a type of chronic myeloid leukemia (CML). Recent data marking 4.5 years of use showed that more than 90% of patients taking Gleevec for this condition continued to survive and were free from progressing to advanced disease. A five-year update from the IRIS study (International Randomized Interferon versus STI571), the largest clinical trial to date for newly diagnosed adult patients with CML, will be presented at the American Society of Clinical Oncology meeting on June 3. Before Gleevec was available, about 50% of patients with this disease progressed to the more advanced stages of CML after only three to five years and survival was generally short for those patients. Traditional, less-targeted treatments were associated with significant toxicities that often limited the ability of patients to stay on therapy long-term. However, Gleevec has an unprecedented record of efficacy and safety for the treatment of patients suffering from CML. "What Gleevec tells us is that a precise understanding of what drives the growth of a particular cancer allows us to target those abnormalities specifically and develop an effective, durable and well-tolerated treatment," said Brian Druker, MD, JELD-WEN Chair of Leukemia Research at the Oregon Health and Science University Cancer Institute, Howard Hughes Medical Investigator and lead investigator of the key Gleevec clinical trials. "After five years, we know with certainty that going after the root cause of a cancer, and shutting it down, not only makes sense - it works." Gleevec’s developer, Novartis, has continued to investigate Gleevec for use in treating patients with other types of cancer. In 2002, Gleevec was approved worldwide for the treatment of patients with unresectable and/or metastatic Kit (CD117)-positive gastrointestinal stromal tumors (GISTs). In 2005, Gleevec was also submitted in the US and EU as a treatment for the solid tumor dermatofibrosarcoma protuberans and certain forms of myeloproliferative disorders as well as for the treatment of adult patients with Ph+ acute lymphoblastic leukemia (ALL). This year, Novartis submitted additional applications for the use of Gleevec in treating two rare hematologic malignancies: hypereosinophilic syndrome and systemic mastocytosis. All five of these diseases are considered rare but may be life threatening and often have no approved treatments.
Scientists Spot Cancer's 'Shield' U.S. scientists say they've discovered a key mechanism by which cancer cells evade detection and destruction by the immune system. The finding could lead to drugs that effectively rob tumors of the protected environment they need to survive and thrive. A molecule called interleukin-23 (IL-23) "creates an environment that's just not acceptable to normal immune surveillance. Healthy immune cells that could kill the tumor can't get in there because of this -- it's almost a shield around the tumor," explained study co-author Robert Kastelein, a distinguished research fellow at the Schering-Plough Research Institute in Palo Alto, Calif., part of the Schering-Plough pharmaceutical company. He and his colleagues published their findings in the May 11 issue of Nature. The California team has for years focused its efforts on the connection between chronic inflammation of tissues and cancer. "This association has been observed for over 100 years," noted senior study author Dr. Martin Oft, senior principal scientist at the institute. He pointed out that sites of chronic inflammation -- such as stomachs affected by ulcers or bowels plagued by Crohn's disease -- are also at high risk for cancer. Pro-inflammatory molecules called cytokines are intimately involved in these processes, and literally thousands of scientific papers have been written about one such cytokine, interleukin-12 (IL-12). But about five years ago, Kastelein's lab discovered that IL-12 was structurally linked to a second, then-as-yet-undiscovered cytokine, IL-23. "Slowly, we began to realize that the chronic inflammatory [role] that had been assigned to IL-12 actually needed to be assigned to IL-23," he said. Besides rewriting the textbooks on IL-12, the finding suggested IL-23 might have a role to play in promoting cancer. In their latest study, the researchers attempted to induce cancer in mice genetically engineered to lack either IL-12 or IL-23. "It turns out that the animals that did not have IL-23 were now protected from tumors," Oft said. "We tried to induce tumors in those mice and they did not get them." Normal mice developed cancers at expected rates, and mice lacking IL-12 actually got more cancers than expected, suggesting that IL-12 -- once considered a cancer villain -- might actually counterbalance IL-23 to help ward off malignancy. According to the California team, the evidence now points to the pro-inflammatory cytokine IL-23 as the "missing link" connecting inflammation and cancer. But how does it do so? The researchers pointed out that the body's immune system is constantly on the alert for rogue cancer cells, killing them wherever they are found. However, in other experiments, Oft and Kastelein found that high production of IL-23 kept immune system "killer" T-cells away from malignant cells, allowing cancer the space and time it needed to grow. On the other hand, suppressing IL-23 brought T-cells flooding back to the tumor site, where they got busy hunting down cancer cells. The bottom line: "If you happen to have chronic inflammation, and IL-23 is fueling that inflammation, your level of immune surveillance is limited," Oft said. "It's a devastating blow to the surveillance of cancer." The discovery of IL-23's crucial role in this process may pump new life into the search for an effective immune-targeted anti-cancer therapy, the researchers said. In fact, Oft said, "we found that if you knock out the receptor for IL-23, animals have a much better chance to control tumor growth. That was very promising." Kastelein said his team is "going full steam ahead" with animal studies that should expand on the IL-23-cancer link. The ultimate goal is the development of immune-based anti-cancer therapies. "One of the key things that's missing now in terms of tumor treatments is how we can use the immune system to attack a tumor," he said. "The problem has been tumor penetration -- nobody has been able to effectively change the tumor environment so that your immune system, which should be able to take care of cancer, can actually do that." But, according to Oft, the idea now is to suppress or otherwise manipulate IL-23 to "ramp up the immune system" and allow T-cells access to vulnerable cancer cells. "We're very upbeat about potential applications further [down the line] in clinical trials," he said.
Targeted Therapies – A Summary A better understanding of the biology of cancer cells has led to the identification of the genes, proteins, and pathways involved in cancer cell growth, survival, and metastasis. During the last decade, therapies that target these specific characteristics of cancer cells have been developed, and these therapies represent a new type of cancer treatment. The American Society of Clinical Oncology has put together this summary of the types of targeted therapies under development and the ones currently approved by the FDA.
New Understanding of Ewing’s Sarcoma Suggests Novel Treatment Strategy Washington, DC, June 2006. Using molecular and cell-based models, researchers at Georgetown University Medical Center have refined the picture of how a cancer-promoting protein associated with Ewing’s sarcoma functions. And in the process, they have hit upon a possible strategy for treatment of the cancer, which is a rare and highly malignant cancer that most often strikes teens and young adults.
In the June 1st issue of the journal Cancer Research, published by the American Association for Cancer Research, the researchers report that the oncoprotein, EWS-FLI1, teams up with a helicase protein that bends the shape of RNA, and together they work to promote or repress transcription of various other proteins, leading to cancer development.
But because it is not possible to directly shut down helicase proteins, given their vital general role in protein transcription, and given that no one has figured out how to clinically inactivate EWS-FLI1 alone, the researchers propose driving a wedge-like drug between the two proteins that would eliminate their interaction.
“Proteins are three-dimensional structures, and the space between EWS-FLI1 and the helicase might be targetable by a small molecule that keeps the proteins apart,” says the study’s lead author Jeffery Toretsky, MD, associate professor in the Departments of Oncology and Pediatrics at the Lombardi Comprehensive Cancer Center. “It could render EWS-FLI1 harmless while not affecting its partnering helicase protein.”
Toretsky adds that the findings may also help explain the workings of a number of difficult-to-treat sarcomas that are caused by the same sort of genetic rearrangements seen in Ewing’s sarcoma. “Understanding the molecules EWS-FLI1 interacts with may provide insights into similar diseases,” he said. “Very little work has been done to study the functional partners of these translocation proteins, and this study may offer a new research approach.”
Ewing’s sarcoma results in solid tumors in bone or soft tissue and is caused by a translocation between two chromosomes which fuses the EWS gene from chromosome 22 to the FLI1 gene of chromosome 11. This fusion produces the EWS-FLI1 fusion protein which is only found in tumors. This translocation is present in 95 percent of tumors, according to Toretsky, a recognized expert on Ewing’s sarcoma. Chromosomal translocations are the cause of many sarcomas and leukemias, and the resulting fusion proteins represent targets for new therapies.
The potential for a drug that would target the fusion proteins in tumor cells was first put forward by scientist Paul Ehrlich more than 100 years ago. In Ewing’s sarcoma, the proteins that are created from chromosomal translocations are unique and only occur in the tumor cells.
Therefore, fusion protein produced by translocation in Ewing’s Sarcoma represents “an ideal target” for therapy, according to Aykut Üren, MD, PhD, assistant professor of oncology at Georgetown and a co-author on the paper. Previously published animal studies using “antisense” molecules have indeed shown that when the EWS-FLI1 is inactivated, Ewing’s Sarcoma does not develop. But antisense, which modifies gene expression, is technologically inappropriate for human therapy, and to date, no one has been able to design a drug that would shut down EWS-FLI1 in humans. “The fusion protein is known to be oncogenic, but we suspected that it must work with other molecules, and these molecular interactions could offer us opportunities for treatment,” Toretsky said.
To find out if their hypothesis was true, the research team utilized a virus that displayed random, but identifiable, protein sequences and mixed the viruses with EWS-FLI1. “We wanted to see what viruses stuck to the EWS-FLI1 protein,” Toretsky said. They found a certain peptide sequence attached to EWS-FLI1 in every experiment they conducted, and a search of the Human Genome database showed these sequences belonged to RNA helicase A (RHA), a common helicase not known to be oncogenic.
They then conducted a number of rigorous studies to prove that EWS-FLI1 and RHA did indeed bind to each other in a complex. Furthermore, when EWS-FLI1was expressed along with RHA, the cells demonstrated increased hallmarks of cancer development.
“The two proteins appear to work together in order for EWS-FLI1 to have maximal oncogenic potential,” Toretsky said. “Since EWS-FLI1 needs RHA, our goal is to keep them apart.”
The study was funded by The Children’s Cancer Foundation of Baltimore, Md. Co-authors include Jeffrey Parvin of Harvard Medical School, Sean Bong Lee of the National Institutes of Health, and Timothy Cripe of Children’s Hospital of Cinncinati.
Search For Cancer Genes Unlikely To Succeed, Say Experts The hunt to find common genes that are associated with cancer is unlikely to be successful, say experts in May 13, 2006 issue (Vol. 332, No. 7550) of the British Medical Journal. Huge resources are being invested in the search for common inherited genetic variants that increase susceptibility to cancer. But devoting a large research effort to searching for common cancer susceptibility genes has several problems, claim authors Stuart Baker and Jaakko Kaprio. The first is that recent research suggests these genes are unlikely to exist or, if they do, are unlikely to have much of an effect on the incidence of cancer. A second reason to play down the role of common susceptibility genes is studies suggesting that environmental, dietary, or lifestyle changes have a large effect on the incidence of cancer. A final reason to be skeptical comes from results from a study of cancers in twins. By analyzing data from identical and non-identical twins, the authors showed that genetic susceptibility made only a small to moderate contribution to the incidence of cancer. The authors claim that prior studies that have shown links between common genes and cancer may be due to bias. But, even if susceptibility genes were identified, showing clinical benefit would still be difficult, and further large trials would be needed, they add. “The search for common cancer susceptibility genes faces important methodological and practical challenges for cancer prevention, given the small chance that such genetic variants exist and the difficulty and expense of proving substantial clinical benefit if they do exist," they conclude. "Enthusiasm for this new field of research should not precipitate unwarranted expectations." Access to the full text of the British Medical Journal can be found by clicking here with a subscription or payment.
NCCN Announces Important Updates to Soft Tissue Sarcoma GuidelinesThe National Comprehensive Cancer Network (NCCN) has announced updates to the NCCN Soft Tissue Sarcoma Guidelines. The NCCN Clinical Practice Guidelines in Oncology(TM) are widely recognized and applied as the standard for clinical policy in oncology in both the community practice setting and in academic cancer centers. These guidelines are used extensively by managed care companies and by Medicare as the basis for coverage policies. These guidelines are updated continually and are based upon evaluation of scientific data integrated with expert judgment. The NCCN Soft Tissue Sarcoma panel recently updated the guidelines to version 2.2006 due to the FDA approval of sunitinib malate (Sutent, Pfizer), a small molecule receptor tyrosine kinase (RTK) inhibitor, for the treatment of gastrointestinal stromal tumor (GIST) after disease progression on or intolerance to imatinib mesylate (Gleevec). Efficacy and safety in GIST patients were evaluated in a randomized, double-blind placebo-controlled trial in patients who had disease progression during prior imatinib treatment or who were imatinib-intolerant. A planned interim efficacy and safety analysis demonstrated a statistically significant advantage for sunitinib over placebo in the primary endpoint of time to progression, as well as in the secondary endpoint of progression-free survival. The panel thus added sunitinib to the guidelines as a treatment consideration for patients with progressive disease. Version 2.2006 of the NCCN Soft Tissue Sarcoma Guidelines can be accessed by clicking here.
A Cup of Cocoa Day May Keep the Doctor Away Harvard University researchers, backed by candy producer Mars Inc., recently released the results of a 10-year study revealing that cocoa, a traditional Jamaican drink, can substantially reduce the risk of heart disease and cancer. The study involved a tribe of Indians called the Kuna. Some of these people live in Panama while others live on islands called the San Blas islands just off the coast of Panama. Researchers compared the causes of death in these two groups. A big difference between the groups was that the Panama Kunas did not consume cocoa regularly, while the San Blas Kunas drank four to five cups of cocoa water per day. The study revealed that the San Blas Kunas, who drank the cocoa water, had a 1,280 per cent lower risk of death from heart disease than the Panama Kunas, and a 630 per cent lower risk of death from cancer. Cocoa is rich in substances called flavanols, a type of polyphenols, which are chemicals that have an antioxidant effect on the body. This means they can 'destroy' free radicals - charged particles, produced by the body, which can damage cells, cause inflammation and trigger diseases like cancer. Dr. Chang Yong Lee and colleagues at Cornell University in New York carried out tests to measure antioxidant levels in tea, red wine and cocoa. A cup of cocoa came out on top in their study, suggesting that it was richer in antioxidants than a glass of red wine or a cup of green tea. But don't leap to conclusions and think that chocolate candy and drinks are good medicine. Yes, cocoa is a major ingredient in commercial chocolate products but most chocolate drinks and candy contain large doses of sugar and milk fat to make them sweet and delicious. Eating milk chocolate bars, for example, will not help you prevent cancer or heart disease because adding dairy products and lots of sugar to chocolate effectively cancels out the healthy antioxidants in the cocoa itself. A good rule of thumb is to consume chocolate containing a minimum of 70 per cent pure cocoa. Avoid added sugars, artificial sweeteners and milk fat to truly gain the natural anti-cancer benefits of cocoa. The best form in which you can consume cocoa is its most pure form: raw cacao. Cacao is the actual bean that cocoa comes from, and it is one of the richest food sources of flavanols available. The best cocoa is natural cocoa powder or the compressed chocolate sticks sold in the market. The studies also show that drinking cocoa as a hot beverage provides the best health benefits. While consuming cocoa on a regular basis will indeed help you significantly reduce the risk of cancer and heart disease, remember that it is not your only option. A wide variety of foods and beverages contain flavanols: green and black tea, pomegranate, cherries, apples, apricots, blackberries, raspberries, purple grapes, callaloo, kale and other greens. However, for cocoa lovers, the word is out: Your favorite food has finally been proven to help prevent cancer and heart disease.
Meetings and Events Each week the journal Nature publishes a free audio show in MP3 format. Nature is a weekly international journal publishing the finest peer-reviewed research in all fields of science and technology, including cancer research. Each podcast show features highlights from news and articles published in Nature, including interviews with the people behind the science with in-depth commentary and analysis from journalists covering the research. A list of previous podcasts is given on the site. You can also subscribe to Nature’s free RSS feed, and then every week when the Nature podcast is published, it'll be delivered straight to your desktop.
Targeted Cancer Therapy Program to air on Public Television For dozens of years, the most common forms of cancer treatments included traditional chemotherapy, radiation and possibly surgery. Now newer medications are emerging, thanks to advances in science. Research has brought about a better understanding of cancer on a molecular level. This understanding is resulting in medicines that zero in on properties unique to cancer cells, allowing those medicines to selectively affect cancer with the potential of less collateral damage to healthy cells in the body. This episode, "Targeted Cancer Therapy," describes how targeted therapies work, and introduces patients and families who are finding hope and healing where there once was none. Produced in association with GIST Support International (GSI, an all-volunteer, non-profit organization dedicated to outreach and education of patients affected by Gastrointestinal Stromal Tumor, and their families and friends. Healthy Body, Healthy Mind airs nationally on public television. For more information, to view the show, or for air dates and times please click here.
16th International Congress on Care of the Terminally Ill
This conference will be
held September 26-29, 2006 in
ASCO Annual Meeting – Sarcoma Sessions The American Society of Clinical Oncology (ASCO) will have its annual meeting on June 2-6 in Atlanta, Georgia. ASCO’s website has published here a list of the oral abstract presentation sessions, education sessions, poster sessions, and clinical science symposia which deal with sarcoma that will take place at this annual meeting. In addition to presentations of the latest sarcoma research and clinical trial results, full sessions are dedicated to the state of the art in osteosarcoma treatment, gastrointestinal stromal tumors, and mTOR molecular targeted therapies.
Tour to Cure Sarcoma Bike Ride On Saturday June 17, 2006, the Tour to Cure bike ride will take place in the Amish countryside of Hills, Iowa. The Tour to Cure is inspired by Seth Bailey who succumbed to soft-tissue synovial sarcoma after a nearly eight year battle. The ride will occur during the Amish “chore hour” (the early evening), and there are two routes – an 18 mile route and a 28 mile route for more experienced riders. The routes will be marked per mile and riders may choose to turn around at any point to return to the starting point of Hills Park. The organizers of this event have a goal of raising $30,000. Team formation and competition to raise donations are highly encouraged. The team and individual who collect the most donations will be honored in the “Yellow Jersey Ceremony.” All proceeds will be donated to the University of Iowa Hospitals and Clinics, and all contributions are tax deductible. Live entertainment and food will provided during the ride. Registration is available online.
Sarcoma Alliance Spirit of Survival Walk in New York City Meet at Arthur Ross Pinetum in Central Park on June 18th at 8:00 am. The area is on the south side of the reservoir, one block north of the Metropolitan Museum of Art which can be accessed through the 5th Avenue or East 96th Street entrance. The 'official' walk/run will start at 9:00 am. The Pinetum is south of the reservoir and south of the 86th St. transverse.
Cancer When You Least Expected ItAn Evening Of Information For Young Adults With Cancer, Gilda’s Club Westchester, 80 Maple Avenue, White Plains, NY, 10601, June 14, 2006 ~ 5:30-8:00 PM, DINNER PROVIDED, Keynote Speaker: Jodi Sax, Founder of the New York LifeLab, Jodi will tell her story of being diagnosed with cancer as a young adult, and the unique challenges she faced after recovery. She went on to develop the New York LifeLab, a comprehensive support community for young adult cancer survivors in their 20’s and 30’s. Following the Keynote Speaker there are two breakout workshops. Choose from the following: Know Your Rights! Employment Issues When You Have Cancer, Fertility Options Before and After Cancer, Moving On: Managing the Psychosocial and Emotional Aspects of Having Cancer as a Young Adult, Sexuality and Reproductive Options For Men, and Body Image After Cancer.
Third Annual Ellen C. McCullough Golf Classic The Third Annual Ellen C. McCullough Golf Classic will be held on June 5 at Bergen Hills Country Club in Rivervale NJ with a lunch following at Seasons in Washington Township. The event will begin at 8 am with a shotgun start. Prizes will be awarded, lunch follows at 1PM at Seasons. Lunch attendees are welcome to participate in a gift basket raffle and 50/50 drawing. Ellen C. McCullough was active in the community and touched people's lives through her kindness toward others and joy of life. She passed away of a rare cancer called LEIOMYOSARCOMA. All proceeds from the outing will support cancer research. Dr. Keohan from Memorial Sloan Kettering along with her Clinical Trials Nurse will be attending the luncheon. In establishing the Outing and luncheon there were three goals 1) To celebrate Ellen's life 2) To teach others about LMS and bring awareness towards this disease 3) To raise money for Cancer Research. For more information , please call 201-391-4757 of E-Mail Kathy McCullough.
Walkers raise $100k to fund Jennifer Hunter Yates Sarcoma Foundation A total of $100,000 was raised for the Jennifer Hunter Yates Sarcoma Foundation at the second annual "12,402 Steps to Cure Sarcoma" Walk, Saturday, May 6. "Funds are still coming in," said Chris Yates, brother-in-law of the 33-year old Hudson woman who is memorialized in the event, "and we have already topped last year's figure of $85,000." He estimated there were at least 350 walkers on the three-mile/ six-mile routes, including the Carmela Farley School fourth-grade class of teacher Robert Yates, whose wife died of the rare form of cancer in April 2004. The students also visited the State House in Boston and obtained a proclamation naming April 30-May 6 "Sarcoma Awareness Week." They collected money for the Yates Foundation, and walked as a group wearing T-shirts announcing their team name - "Yates' Small Feet- Big Hearts." Massachusetts General Hospital staff doctors and family members addressed the crowd assembled for the walk, thanking them for their support. Dr. David C. Harmon of the MGH Cancer Center said that the $75,000 raised in the initial Yates Foundation walk last year, "has already had impact on sarcoma patients and families at MGH." He said a sarcoma research team has been organized to better enable patients to participate in clinical trials. An "Innovations in Sarcoma Seminar Series" will educate patients and families about current treatments, and allow patients and families to connect with one another. He said that Yates Foundation funds have also created a user-friendly Web page to assist patients in the treatment and management of their disease.
Northwest Sarcoma Foundation's Dragonslayer Bike, Hike or Trike Event Karen Murphy, Executive Director pf the Northwest Sarcoma Foundation, recently reported that their 2006 Sarcoma Dragonslayer Bike, Hike or Trike, which was held on May 6, 2006, exceeded their fundraising goal of $50,000 this year. In fact, they reached a little over $60,000, and had 400 participants. It was overwhelming and inspiring to see all the familiar faces, as well as meeting our new friends. Please view their photo album from the event by clicking here.
End Notes The June 2006 issue of CureXtra can be viewed by clicking here.
GoodSearch is an Internet search engine with a simple concept and unique social mission. GoodSearch enables you to help fund any of hundreds of thousands of charities or schools through the simple act of searching the Internet. The company was founded by a brother and sister team who lost their mom to cancer and wanted to find an easy way for people to support their favorite causes. It's simple. You use GoodSearch.com like any other search engine (GoodSearch has partnered with Yahoo Search to ensure the best results), but each time you do, money is generated for your favorite cause. The more people who use this site, the more money will go to your favorite cause. How does it work: (1) On the GoodSearch homepage, choose from hundreds of thousands of organizations or add your favorite cause to our list; (2) Search the Internet just like you normally would; (3) Fifty percent of the revenue generated from advertisers is shared with the charity, school or nonprofit organization of your choosing. GoodSearch estimates that each search will generate approximately $0.01 for the designated charity or school. If you think about how many times you search the Internet each year, and then add in all the searches from the supporters of your organization, it can quickly add up! There is no cap on how much money GoodSearch will direct to charities. Users do not have to pay anything to use GoodSearch, thus GoodSearch now provides all Internet users with an easy way to donate to their favorite charities without ever having to tap into their own finances. It is easy to add your organization to the GoodSearch list of charities, and one can track the number of searches and revenue raised by a particular charity. GoodSearch asks that you use the site honestly as fraudulent searching will result in the charity being de-listed.
V3N3 ESUN Copyright © 2006 Liddy Shriver Sarcoma Initiative.
|
