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http://www.prnewswire.com.br/news/080500000151.htm Excerpt from article: . . . . . . . . . Lung cancer patients whose histology is factored into treatment decisions may fare better as a result, according to data from a pivotal non-small cell lung cancer (NSCLC) clinical trial. Data from the trial, which involved Eli Lilly and Company's ALIMTA® (pemetrexed for injection), will be presented at the 44th Annual Meeting of the American Society of Clinical Oncology (ASCO) in Chicago, Ill., May 30 --- June 3, 2008). "The data presented at ASCO confirms that histology matters when treating non-small cell lung cancer," said Richard Gaynor, M.D., vice president, cancer research and global oncology platform leader for Lilly. "We are seeing continued affirmation that when physicians factor in a patient's histology, pemetrexed becomes an even more valuable treatment option in non-small cell lung cancer." Results from a multicenter, double-blind Phase III trial will be presented on June 2, 2008, at ASCO (Abstract # 8011). The study also was one of those featured during ASCO's live online presscast, a virtual press event that marked the first time researchers were invited to present key abstracts to the media prior to the annual meeting. The trial compared the efficacy and safety of pemetrexed versus a placebo in 663 patients with stage IIIB/IV NSCLC whose disease had not progressed after four cycles of platinum-based induction chemotherapy. According to the results, patients treated with pemetrexed demonstrated increased efficacy with respect to progression-free survival compared to those treated by placebo (4.3 months vs. 2.6 months), and pemetrexed patients also achieved better tumor response (p < 0.001). However, when data was broken down by histology, it was comparable to previous pemetrexed trials evaluating histology -- patients with a non-squamous histology fared better than those with a squamous histology. Patients with non-squamous histology who were treated with pemetrexed achieved 4.5 months of median progression-free survival compared to 2.8 months for patients with squamous histology. "The efficacy findings of this data show that pemetrexed performed better in patients with non-squamous histology for the treatment of non-small cell lung cancer," said the trial's lead investigator, Tudor Ciuleanu, M.D. of the Institutul Oncologi I Chiricuta in Cluj, Romania. Patients in the trial were treated with pemetrexed (500 mg/m2) plus best supportive care or placebo plus best supportive care. All patients were supplemented with vitamin B12, folic acid and dexamethasone. No significant toxicity differences were identified between the two trial arms with the exception of grade 3/4 anemia (pemetrexed 4.5%, placebo 1.4%) and total serious adverse events due to the treatment (premetrexed 4.3%, placebo 0%). The data presented at ASCO reaffirmed findings from previous studies, most notably a Phase III study of pemetrexed plus cisplatin versus gemcitabine plus cisplatin in chemonaive patients with locally advanced or metastatic NSCLC. That study showed NSCLC patients with a non-squamous histology (those with adenocarcinoma or large cell carcinoma demonstrated increased benefits when treated with premetrexed(1). . . . . . . . . . (PRNewswire/First Call, May 15, 2008, [Contains Forward-looking Statements]) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

http://health.usnews.com/articles/healt ... -lung.html Excerpts from article: . . . . . . . . . A panel of 15 genes may help determine which patients with early-stage non-small cell lung cancer will experience a recurrence and, therefore, benefit the most from chemotherapy, a new study shows. . . . . . . . . . By extension, the same genetic signature may also identify patients with less aggressive forms of the cancer who would be able to forego chemotherapy. "Using this signature, we can identify up to 30 to 40 percent of stage I patients who might benefit from post-surgery chemotherapy and maybe up to 30 to 40 percent who might not benefit," said study author Dr. Ming Tsao, who will present the finding June 1 at the American Society of Clinical Oncology (ASCO) annual meeting, in Chicago. "The idea is that this could potentially supercede staging, although we definitely need more studies. [The information] is not immediately useful." Previous trials have shown a benefit for stage I and II non-small cell lung cancer patients who received chemo after surgery. But, so far, the benefit has been confined mostly to stage II patients. Even so, the distinction is not clear-cut. Some 30 percent of stage I patients who don't get added chemotherapy will die of a disease recurrence, and it's also possible that some stage II patients might not need chemotherapy after surgery. "The goal of this study was to identify the genetic characteristics that could potentially be used to predict more precisely the likelihood of clinical outcomes, so those who need post-surgery chemo should get it and those who do not need it do not get it," explained Tsao, who is professor of laboratory medicine at the University of Toronto and a senior scientist at Princess Margaret Hospital in Toronto. Gene expression profiling was performed on frozen tumor tissues from 64 patients as part of a follow-up analysis of a National Cancer Institute of Canada trial. Researchers then identified a group of 15 genes that divided the patients into high-risk (33 patients) and low-risk (31 patients) categories. The signature was then validated in five other databases comprising a total of 372 stage I and II lung cancer patients. Chemotherapy reduced the risk of death in high-risk patients (both stage IB and stage II) by about 67 percent, but not in low-risk patients. While a previous analysis showed that overall, only patients with stage II disease benefited from chemotherapy after surgery, this study has demonstrated that the 15-gene signature may identify patients with both stage I and II cancers who would benefit from postoperative chemotherapy, further supporting its use in the selection of appropriate treatments. In other news from the meeting, scientists from the University of Medicine and Pharmacy Iuliu Hatieganu in Romania have demonstrated for the first time that maintenance therapy (given after standard "induction" chemotherapy) with the chemotherapy drug Alimta (pemetrexed) extended time to recurrence by 50 percent. "The data revealed a remarkably statistically significant 40 percent reduction in the risk of progression with pemetrexed, and a doubling of the median progression-free survival," said study author Dr. Tudor Eliade Ciuleanu, an associate professor at the University of Medicine and Pharmacy Iuliu Hatieganu in Romania. The study involved 663 patients with advanced non-small cell lung cancer who had already undergone the initial course of chemo. Eli Lilly, which makes the drug, was involved in the trial. Patients who received Alimta lived for 4.3 months without a recurrence of the disease, versus 2.6 months for those taking a placebo. Overall survival was 13 months in the Alimta group as compared with 10.2 months in the placebo group. Finally, a Duke Comprehensive Cancer Center study found that post-surgical lung cancer patients can do well with aerobic exercise regimens starting as little as one month after surgery. Twenty individuals newly diagnosed with and who had undergone surgery for Stage I to Stage IIIb lung cancer were asked to exercise three times a week for one hour at a time on stationary bikes. After 14 weeks, participants reported being less tired and also had more aerobic fitness (as measured by oxygen levels after exercising). . . . . . . . . . (HealthDay News, By Amanda Gardner, HealthDay Reporter, [More Information: NCI, May 16, 2008]) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

http://www.sciencedaily.com/releases/20 ... 123855.htm: Excerpt from article: . . . . . . . . . Patients who have undergone surgical procedures for the removal of lung cancer can tolerate and benefit from exercise regimens started just a month after surgery, according to a new study led by researchers at the Duke Comprehensive Cancer Center. "Previous studies have demonstrated that exercise can benefit cancer survivors but lung cancer patients have been a particularly challenging group, because surgery on the lung was perceived to have a restrictive effect on the amount of exercise a person can do," said Lee Jones, Ph.D., a researcher at Duke and lead investigator on the study. "Our study showed that this population can not only tolerate exercise but that it can lead to improved tolerance for exercise, and better quality of life." This study lays the foundation for future studies looking at the effect of exercise on survival in lung cancer patients, Jones said. This study followed 20 newly diagnosed lung cancer patients, who had undergone surgery. Participants had been diagnosed with Stage I to Stage IIIb cancer. The patients were expected to participate in three hour-long exercise sessions per week, on stationary bikes. The study lasted 14 weeks. The attendance rate for the exercise sessions was nearly 85 percent, and patients were less fatigued and gained greater aerobic fitness over the course of the study, as measured by what is known as a "maximal exercise test," similar to the type Lance Armstrong performed prior to riding in the Tour De France. The test involves having a participant pedal until he can no longer tolerate it, and then measuring his oxygen levels by asking him to breathe into a device. "What we found is that patients can stick with the regimen, and that they are functioning a lot better as a result," Jones said. "Investigating the most effective type of exercise on changes in exercise tolerance, uncovering the mechanisms underlying these changes, and whether these changes can impact long-term survival will be the subject of subsequent studies." Study participant Danny Robbins said that being part of this study has helped him develop an exercise habit, which he hopes will help him continue to beat lung cancer, as well as combat his high blood pressure and diabetes. "Before I participated in this study, I struggled with walking in the neighborhood with my wife," Robbins said. "Now, I exercise five days a week and it's gotten to the point that I don't feel like I have to do it; rather, I feel like I don't want to miss it." . . . . . . . . . (Science Daily, Research News, May 16, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

http://www.sciencedaily.com/releases/20 ... 171029.htm ARTICLE: . . . . . . . . . In an effort to better define and ultimately address fatigue more effectively, a qualitative study from The University of Texas M. D. Anderson Cancer Center has identified three primary themes - loss of strength or energy, major effects of fatigue and associated sensations - among patients being treated with standard radiation therapy. Presenting at the 33rd Annual Congress of the Oncology Nursing Society (ONS), Loretta A. Williams, Ph.D., RN, AOCN, OCN, an instructor in the Department of Symptom Research at M. D. Anderson, detailed commonalities of 21 patients who shared personal stories of dealing with cancer's most distressing and common symptom. "While fatigue is a well-recognized symptom of cancer and its treatment, the measurement of fatigue has been based on many different ideas and definitions. Few of these definitions have included patient input. We're trying to define fatigue based on patient experience," said Williams. "Once we're able to determine the critical elements of fatigue, we'll be better equipped to ask the right questions of patients to assess fatigue. Healthcare professionals - including nurses - will be in a much better position to intervene with patients to manage or prevent fatigue." The study included open-ended, audio-taped interviews with 21 patients, all who were receiving radiation therapy at M. D. Anderson. The patients were evenly divided with diagnoses of breast, prostate and head and neck cancer. Of the 21 patients who were interviewed during the fifth week of radiation therapy, 57 percent were women and the average patient was 54 years old. In the study, patients reported a loss of strength or energy that included feelings of tiredness or weakness, which may progress to exhaustion, and lack of energy and stamina. Because of the qualitative technique that Williams and her team used, their dialogues with patients revealed comments such as, "I don't have a body part that is tired. My whole body is tired," "I just have a weak feeling...pretty well all over," and "Fatigue to me is just a feeling of no energy." More than 85 percent of the patients in Williams' study used the terms, "tiredness" and "lack of energy" to describe fatigue. According to the researchers, these may be good terms for patients to use when speaking with health care providers about fatigue and terms that should alert the providers to patients experiencing it. The team also reported that the effects of fatigue included a lack of motivation or inability to perform usual activities, decreased interest in social activities, and an overwhelming need to rest at times. "Among the patients that we talked to, they often expressed an inability to do things that they could easily do before their treatment or before their diagnosis," said Williams. "They frequently reported that they didn't want to be around others, that it took too much out of them to keep up a conversation or be cordial." Williams and her team also pinpointed physical sensations associated with fatigue that included, "malaise, aching, feelings of heaviness or weight, slowness of movement, lack of appetite, and mental sensations of psychological distress and difficulty thinking or concentrating." One patient described the physical sensations as "a feeling of heaviness," while another said, "I just felt myself dragged out, just tired, and it was distressing to me because that's not my norm. I don't like to feel like that." "Defining the patient's experience with a symptom is critical to assessing and managing that symptom," said Williams who was a clinical nurse specialist before joining M. D. Anderson's Department of Symptom Management as a nurse-scientist. "Assessing and managing symptoms, certainly fatigue, is a primary role of oncology nurses." Williams and her team are planning similar future studies to better define fatigue among patients receiving chemotherapy and new targeted therapies. They plan to develop a single definition of cancer-related fatigue. Collaborating with Williams on the study were Shannon Burkett, Ph.D., Margaret H. White, B.A., Ibrahima Gning, Ph.D. and Charles Cleeland, Ph.D. The study was sponsored by a research grant from Cephalon, Inc. . . . . . . . . . (Science Daily, Research News, May 15, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

Congratulations, Nicole, on that really great news. I am so very happy for you. May both of you, enjoy a much-deserved, restful, and fun-filled summer. Barbara

http://www.sciencedaily.com/releases/20 ... 215901.htm ARTICLE: . . . . . . . . . Chemotherapy given in conjunction with cancer vaccines may boost the immune system's response, potentially improving the effectiveness of this promising type of cancer therapy, according to a study by researchers in the Duke Comprehensive Cancer Center. "Chemotherapy first knocks out T regulatory cells that suppress immune function and we speculated that this might have a complementary effect when used in conjunction with vaccines, which work by boosting immune function," said Timothy Clay, Ph.D., a researcher at Duke and a lead investigator on this study. "We tested this theory both pre-clinically and in patients who were part of a vaccine trial at Duke for gastrointestinal cancers, and found that our hypothesis seemed to be true." Researchers used a drug called denileukin diftitox (ONTAK) for this study; the drug is routinely used to treat a type of lymphoma and is known to deplete certain types of immune cells including the T regulatory cells that "put the brakes" on immune function. They speculated it might facilitate better immune responses to a cancer vaccine. "In the lab work, we definitely saw a heightened immune response when we used the denileukin diftitox in conjunction with the vaccine. The vaccine we used targets a protein found in gastrointestinal tumors and works by boosting immune response to the cells carrying that protein," Clay said. "From there, we gave the drug to 15 patients in a phase I study using the vaccine." The researchers found that when multiple doses of the denileukin diftitox were given, immune response to the vaccine was enhanced in these patients. "This is encouraging. The next step will be to develop better drugs that support vaccines by enhancing the immune response they depend on to work," Clay said. "It's a concept that can be applied to any type of solid tumor, which has huge implications for cancer research." Vaccines are being used in clinical trials across the country to treat many malignancies, including lung cancer, brain tumors and colorectal cancer. The researchers will present their findings at the annual American Society of Clinical Oncology meeting in Chicago, on May 31. The study was funded by the National Cancer Institute. Other researchers involved in this study include Amy Hobeika, Takuya Osada, Delila Serra, Donna Niedzwiecki, H. Kim Lyerly and Michael Morse. . . . . . . . . . (Science Daily, Research News, May 16, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

http://www.newswise.com/articles/view/540878/?sc=dwhn ARTICLE: . . . . . . . . . Patients who feel better live longer, say Mayo Clinic researchers, working with the North Central Cancer Treatment Group (NCCTG), in study results released May 15 as part of the 44th Annual Meeting of the American Society of Clinical Oncology (ASCO). Mayo Clinic cancer researcher and the study’s lead author, Angelina Tan, says the results show quality of life is an independent factor in survival. “Quality of life appears to affect the survival of cancer patients,” says Tan. “If physicians can identify patients who are not doing well, they will be able to intervene and, we hope, improve not only their patients’ sense of well-being, but also their length of life.” The researchers compared overall survival with responses from 3,704 patients to one question -- “On a scale of 0 to 10, how would you rate your quality of life?” Patients had a variety of cancer types, and the question was asked during their participation in one of 24 different NCCTG clinical trials. The unifying factor for the patients was that all had late-stage disease. All results were converted to a 100-point scale. The team found that baseline quality of life was a strong predictor of survival. They found a distinct difference when dividing patients by the median score of 83 (6.1 months increased survival time for those with scores greater than or equal to 83). The investigators also divided the group into those with scores of more than 50 and 50 or less, defining those in the 50 or less category as having clinically deficient quality of life. In this analysis, the results were even more striking, with increased survival of 7.5 months for the non-clinically deficient patients. The investigators determined that these numbers were independent of performance status (a traditionally used survival prediction method evaluating a patient’s ambulatory status). This study is one of several similar quality of life studies that are being presented by Mayo Clinic researchers at the ASCO annual meeting. “Quality of life research is a priority at Mayo,” says Jeff Sloan, Ph.D., a cancer researcher at Mayo and the study’s primary investigator. “While doctors know that a patient’s quality of life is important, these studies show that measuring it is necessary and can predict how patients will do.” Dr. Sloan, Tan and their colleagues at Mayo Clinic and NCCTG hope current and future research will identify both how and when clinicians can best support their patients’ feelings of well-being. For example, if the quality of life deficit was identified to be related to patient fatigue and emotional distress, interventions (pharmaceutical, psychosocial, etc.) could be offered to improve patient well-being. “If quality of life deficits can be identified routinely in clinical practice, it will help patients,” says Tan. “Physicians can address the issues leading to a decrease in quality of life, and ideally these interventions will extend survival.” Other researchers included Paul Novotny; Judith Kaur, M.D.; and Jan Buckner, M.D., all from Mayo Clinic. NCCTG researchers included Paul Schaefer, M.D., Toledo Community Hospital Oncology Program, Toledo, Ohio; Philip Stella, M.D., St. Joseph Mercy Health System, Ann Arbor, Mich.; and John Kuebler, M.D., Columbus Community Clinical Oncology Program, Columbus, Ohio. Related quality of life studies being presented at ASCO include: Baseline quality of life is a strong prognostic factor for overall survival in patients with advanced stage non-small cell lung cancer, Schild et al. A quality-of-life assessment of patients participating in phase I clinical trials confirms a decrease during treatment, Atherton et al. Baseline quality of life is a strong and performance status-independent prognostic factor for overall survival in patients with metastatic colorectal cancer, Turja et al. Tumor burden is not related to quality of life in patients with metastatic colorectal cancer, Sloan et al. For more background information on integrating quality-of-life measures into clinical practice, read Mayo’s two-part monograph published in the November–December 2005 and November–December 2006 issues of Current Problems in Cancer. NCCTG is a national clinical research group sponsored by the National Cancer Institute. Its research and administration are based at Mayo Clinic. NCCTG consists of cancer specialists at community clinics, hospitals and medical centers in the United States, Canada and Mexico. The group is dedicated to bringing clinical trials with promising new cancer therapies to communities where patients live. . . . . . . . . . (NewsWise, Medical News, Source: Mayo Clinic, May 16, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

http://www.sciencedaily.com/releases/20 ... 215852.htm ARTICLE: . . . . . . . . . Celecoxib, the anti-inflammatory medication also known by the trade name Celebrex, has proven to be safe and reduces a specific proliferation measurement of precancerous lesions in the lung, according to a study from The University of Texas M. D. Anderson Cancer Center. This finding demonstrates the significance of COX-2 inhibition toward preventing lung cancer in individuals at higher risk of developing the disease. The study is the first large randomized trial of Celebrex in lung cancer prevention; the findings will be presented at the American Society for Clinical Oncology's (ASCO) upcoming annual meeting as an oral presentation. "With this study, in principal, we've been able to demonstrate the importance of COX-2 and the implications on inflammation pathway in lung cancer development," said Edward Kim, M.D., assistant professor in M. D. Anderson's Department of Thoracic Head and Neck Medical Oncology. "We've also been able to demonstrate that this drug class is safe and tolerable for this patient population. As we move forward in lung cancer chemoprevention, the importance of this class of drugs cannot be ignored." From November 2001 to September 2006, the M. D. Anderson study enrolled 212 individuals, all of whom were current or former smokers with at least a 20-pack-year smoking habit. Most participants did not have any history of cancer; however, patients with a history of cancer who had been disease-free for six months could participate. The median age of participants was 53. The study examined levels of KI-67, a biomarker associated with precancerous lung lesions. Participants underwent a baseline broncoscopy in which six predetermined biopsies were performed. They then were randomized to receive Celebrex at either 200 milligrams (low dose) or 400 milligrams (high dose) twice a day or placebo. After three months, participants received a second broncoscopy, the primary endpoint of the trial. Patients had the option to continue on the trial for three more months per their prior randomized arm; for those participants, a third and final broncoscopy was conducted at six months. "In patients who had high risk features such as smoking, especially in the current smokers, we were able to see that a higher dose of Celebrex could decrease the proliferation marker KI-67 in these patients, as seen through their bronchial epithelium," said Kim. "We are encouraged that we have a drug like Celebrex that decreases the expression of this proliferation marker." These findings are also significant in that the study shows that serial broncoscopies are feasible, explained Kim. "Although CT scanning and other imaging techniques are important, for lung cancer, it may be vital to examine actual tissue to see what the markers are doing in the actual epithelium of the lung so as to best understand if an individual has a higher or lower risk of developing lung cancer." Celebrex is in a class of medications known as nonsteroidal anti-inflammatory drugs (NSAIDs), like aspirin or ibuprofen, which work by blocking chemical enzymes that cause inflammation. The COX-2 enzyme inside cancer cells is thought to control the synthesis of prostaglandins, which are substances believed to trigger cancer cell growth. Researchers believe that prostaglandins promote the growth of new blood vessels to feed tumors, and also protect new cancers from destruction by the body's immune system. Blocking the COX-2 enzyme may reduce the amount of prostaglandin available to cancer cells and thus repress tumor growth, says Kim. In December 2004, M. D. Anderson voluntarily suspended the trial at the request of Pfizer and the National Cancer Institute, the funding source for the study, until further data on the drug's risk for cardiac toxicities, specifically heart attacks and strokes, could be investigated. Months later, advisors to the FDA recommended that Celebrex continue to be studied in the treatment and prevention of cancer, and the NCI supported the continuation of the trials, encouraging investigators to weigh the risks and benefits of the drug for their specific clinical setting. After adding stringent guidelines to further reduce the cardiac risk to patients, the M. D. Anderson investigators then reapplied to the institution's Institutional Review Board to reactivate the trial. The study reopened in May 2005. Kim noted that there were no adverse cardiac events in the M. D. Anderson trial. Three patients experienced grade three toxicities on the higher dose of the drug which were not cardiac related. Lung cancer is the leading cause of cancer death in the United States, according to the American Cancer Society. In 2008, approximately 215,000 people will be diagnosed with lung cancer and approximately 114,000 people will die from the disease. The study was funded by a five-year, $10 million POI lung grant, awarded in 2001 by the NCI to a multi-disciplinary team headed by Waun Ki Hong, M.D., head of the Division of Cancer Medicine. M. D. Anderson has been a leader in chemoprevention since the early 1990s, when Hong was the first to demonstrate that retinoids can reverse oral leukoplakia, a premalignant condition that often leads to cancer, and that 13-cis retinoic acid can prevent secondary primary tumors among patients with head and neck cancers. "Lung cancer remains a lethal and stubborn disease with tobacco as the leading culprit for this killer," said Hong. "The Celebrex findings are exciting for the entire field of lung cancer chemoprevention." In addition to Kim and Hong, other M. D. Anderson faculty members on the study include: Jack Lee, Ph.D., professor in the Department of Biostatistics, Li Mao, M.D. professor in the Department of Thoracic/Head and Neck Medical Oncology-Research, Rodolfo Morice, M.D., professor in the Department of Pulmonary Medicine, Diane Liu, statistical analyst in the Division of Quantitative Sciences; Georgie Eapen, M.D., assistant professor in the Department of Pulmonary Medicine; Ignacio Wistuba, M.D., associate professor in the Department of Pathology-Research and Jonathan Kurie, M.D. professor in the Department of Thoracic/Head and Neck Medical Oncology, who served as Principal Investigator on the Celebrex trial. Updated data will be presented at ASCO on June 2 in the clinical science symposium session "Clinical Testing of Agents for Cancer Prevention: The Price of Progress." . . . . . . . . . (Science Daily, Source: University of Texas M. D. Anderson Cancer Center, May 15, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

Comment: A few years prior to Bill's mother's diagnosis of cancer, she began losing her teeth. She was in her early sixties when this occurred. Several of them seem to have looosened from their moorings. My mother began losing her teeth prior to her diagnosis of colon cancer. She went on to survive Stage IV, but took care to have any inflammation of her gums attended. That is why this article caught my attention. http://www.local6.com/health/16261857/detail.html ARTICLE: . . . . . . . . . People who lose teeth have an increased risk of esophageal, head and neck, and lung cancers, according to Japanese researchers. The authors of the study said that they suspect that infections and inflammation from poor dental care -- which can cause tooth loss -- could also help the cancers develop. After studying more than 5,000 cancer patients and 10,000 people without the disease, the researchers determined there was a 136 percent greater chance of developing esophageal in those who had lost teeth. The rates went up 68 percent for head and neck cancer and 54 percent for lung cancer. The researchers also found that the more teeth someone lost, the greater the chance of cancer. Lead researcher Akio Hiraki, noted that while widespread inflammation could explain the link between tooth loss and cancer risk, they also note that tooth loss in the cancer patients may simply reflect unhealthy behaviors that contribute to cancer risk. Also, people who have lost teeth may not be able to eat a healthy diet, and diet is also a factor in cancer development. . . . . . . . . . (Local6, Health, May 14, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

Dear Gracie, My husband, Bill, went through WBR last year and completed the many treatments in June, 2007. Our son, adopted many decades ago when he was 7 months old, and who presently is a Roman Catholic priest, came here, and gave his father a blessing. Bill's latest MRI, almost one year later, showed that the tumor in the midbrain had disappeared through the WBR treatments. It was gone completely. We do not claim anything, except that we have always believed that prayer, blessings, and spirituality can help. We accept the blessing, and are very grateful. My belief is that we are spirits within our human embodiments, and can be recipients of a greater good. Much love and hope always to you, Gracie, Barbara

http://news.bbc.co.uk/2/hi/health/7396814.stm ARTICLE: . . . . . . . . . A key mechanism by which smoking triggers genetic changes that cause lung cancer has been unravelled. Researchers have shown exposure to cigarette smoke slows production of a protein called FANCD2 in lung cells. This protein plays a key role in repairing damage to DNA, and causing faulty cells to commit suicide before they go on to become cancerous. The study, led by Oregon Health and Science University, appears in the British Journal of Cancer. LUNG CANCER Most common cancer in the world with 1.3 million people diagnosed every year Second most common form of cancer in the UK after breast cancer Over 38,300 new cases, and more than 33,000 deaths in the UK each year Smoking responsible for 90% of cases in the UK It raises hopes of improved treatments for the disease. Lead researcher Dr Laura Hays said: "These findings show the important role FANCD2 plays in protecting lung cells against cigarette smoke and may explain why cigarette smoke is so toxic to these cells." The researchers suspect other proteins also play a role in fixing DNA and weeding out defective cells. However, their work showed that cells with very high levels of FANCD2 were resistant to the toxic effects of smoke - suggesting this protein is key. Artificial windpipe The researchers created an artificial windpipe in the lab to replicate the environment of a smoker's lung. They then studied the effects of cigarette smoke on different proteins in cells and found that FANCD2 levels were low enough to allow DNA damage. FANCD2 is part of a family of proteins involved in an inherited condition called Fanconi anaemia. People with the condition are more likely to develop cancers at a young age and have low levels of these proteins. Dr Lesley Walker, director of cancer information at Cancer Research UK, said: "This interesting piece of science adds to our understanding of why smoking is so deadly. "Smoking is the single biggest preventable cause of cancer and causes nine out of ten cases of lung cancer. "But the good news is that quitting works - after five years without smoking your risk of a heart attack will have fallen to half that of a smoker. "And after ten years your risk of lung cancer will have halved too." . . . . . . . . . (BBC News, May 14, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

http://www.medicalnewstoday.com/articles/107121.php Excerpt from article: . . . . . . . . . GSL Receives Authorisation In Europe For Oral Hycamtin® (topotecan Hard Capsules) For The Treatment Of Relapsed Small Cell Lung Cancer GlaxoSmithKline (GSK) announced that oral Hycamtin® (topotecan hard capsules) have received approval from the European Commission for the treatment of relapsed SCLC. Specifically, topotecan hard capsules are indicated as monotherapy for the treatment of adult patients with relapsed SCLC (PS0-2 [*]) [1] for whom re-treatment with the first-line regimen is not considered appropriate. Topotecan is already available as an intravenous (IV) injection and the approval of topotecan hard capsules provides physicians and patients with another convenient option. "The approval of topotecan hard capsules is welcome news for patients and their physicians. Small cell lung cancer is a very aggressive disease and there are limited treatment options after relapse," said Dr. Mary O'Brien, Head of the Lung Cancer Unit at The Royal Marsden Hospital, Surrey, UK. "Topotecan not only improves symptoms and extends the lives of patients, but as it is in capsule form treatment can be started without delay." "The European approval of topotecan as an oral formulation is good news for patients with relapsed small cell lung cancer across Europe. Topotecan hard capsules provide physicians and patients with an alternative, effective treatment, with the added convenience of being administered orally," said Eddie Gray, President, Pharmaceuticals Europe, GlaxoSmithKline. "The approval of topotecan capsules continues to underscore GSK's commitment to the research and development of therapies to address the unmet medical needs of cancer patients around the world." Data Submitted The approval was based on positive results from a Phase III study comparing topotecan hard capsules plus best supportive care (BSC [†]) to BSC alone in patients with relapsed SCLC, in addition to Phase II and Phase III supporting studies. In the pivotal Phase III multicentre trial, 141 patients with relapsed SCLC not considered as candidates for standard IV therapy were randomised to receive BSC alone [n = 70] or topotecan capsules plus BSC [n = 71]. Topotecan capsules added to BSC were associated with prolonged survival in patients with relapsed SCLC (p = 0.0104, HR = 0.64). Median overall survival for topotecan capsules plus BSC was 25.9 weeks (95% CI, 18.3. to 31.6 weeks) compared to 13.9 weeks (95% CI, 11.1 to 18.6 weeks), indicating a 36% reduction in risk of death for patients who received topotecan capsules plus BSC compared with patients who received BSC alone. [2] During the Phase III study the most common Grade 3 or 4 toxicities with topotecan capsules were neutropenia, anaemia, thrombocytopenia, nausea, diarrhoea, vomiting, fatigue, and alopecia.2 Supporting Studies Submitted Supportive efficacy and safety data were provided from a Phase II and a Phase III study, each of which compared topotecan capsules (oral) directly to topotecan (IV) in patients with relapsed sensitive SCLC. In the Phase III study median survival time was 33.0 weeks (95% CI, 29.1 to 42.4 weeks) in the oral group and 35.0 weeks (95% CI, 31.0 to 37.1 weeks) in the IV group, and both treatments were generally well-tolerated. [3] Safety data were presented for the three efficacy studies mentioned above and for an integrated relapsed lung cancer study population of 682 patients. The safety profile was consistent across all four studies.3, [4], [5], [6] About Small Cell Lung Cancer (SCLC) Lung cancer is the third most common cancer in Europe contributing to 12.1% of all cancer cases, but it is the most common cause of death from cancer, with an estimated 334,800 deaths in 2006 (19.7% of total deaths from cancer). [7] About 20 out of every 100 cases diagnosed are SCLC. Of all those diagnosed with SCLC, around one in three have limited (early) disease at the time of diagnosis. Two in three already have extensive (advanced) disease at the time of diagnosis. Of those who have limited disease and have chemotherapy, between 35 - 40% will be alive two years following treatment. People with extensive disease are also treated with chemotherapy, but unfortunately the survival rate is even lower. Most only survive another 10 to 12 months following treatment. [8] About Hycamtin Hycamtin (topotecan) is a chemotherapeutic agent that belongs to a class of drugs known as topoisomerase I (topo-I) inhibitors. Topo-I is an enzyme essential for the replication of DNA, and therefore cell division, in both normal and cancer cells. Interaction between topo-I and topotecan results in damage to the cell's cancerous genetic material and the death of dividing cancer cells.6 . . . . . . . . . (Medical News Today, Lung Cancer News, May 13, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

http://www.medicalnewstoday.com/articles/107271.php ARTICLE: . . . . . . . . . In a leading study that has implications for the development of novel therapies for a number of breast, lung and ovarian cancers that have lost the expression of a gene called glypican-3 (GPC3), Sunnybrook researchers have discovered how the loss of the GPC3 gene induces overgrowth through certain growth factors such as Sonic Hedgehog which stimulate cancer growth. Published in Developmental Cell, the study examines the molecular mechanism by which lack of functional GPC3 causes overgrowth in the Simpson-Golabi-Behmel syndrome (SGBS), a rare disorder that predisposes to cancers. "This vital new finding at the molecular level opens doors for the development of novel treatments to inhibit overgrowth activity to benefit SGBS patients and the many breast, lung and ovarian cancer patients linked to loss of GPC3," says Dr. Jorge Filmus, senior scientist, Division of Molecular and Cellular Biology, Sunnybrook Research Institute, and the study's lead investigator. Early clinical trials presented at the last annual meeting of the American Association for Cancer Research in which cancer patients are being treated using Hedgehog-inhibitor drugs show promise. GPC3 or glypican-3 is one of six genes of the glypican family. Glypicans are expressed predominantly during development in a stage and tissue specific manner suggesting they play a role in cell growth and in establishing the shape of tissues and organs. . . . . . . . . . (Medical News Today [from original press release], Source: Canadian Institute of Health Research & NCI of Canada, May 13, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

http://www.medicinenet.com/script/main/ ... ekey=89223 ARTICLE: . . . . . . . . . A number of potential new targets for treatments that block tumor blood vessel formation — a key step in tumor growth and metastasis — have been identified by researchers at the University of North Carolina at Chapel Hill. The use of the drug bevacizumab (Avastin) to target the formation of blood vessels (angiogenesis) that feed tumors has proven successful in treating breast and colon cancer, according to background information in the study. The drug inhibits a protein called vascular endothelial growth factor (VEGF), which plays a major role in angiogenesis. "There is a large amount of data that shows if you block angiogenesis, you can block tumor growth. But VEGF is not responsible for all of angiogenesis. We wanted to identify more targets for this therapeutic approach," study senior author Dr. Nancy Klauber-DeMore, an associate professor of surgery in the UNC School of Medicine, said in a prepared statement. She and her colleagues identified new targets after analyzing blood vessel cells in cancerous and normal breast tissue samples. They identified 1,176 genes that differed in activity or expression between the two cell populations. Of those, 55 genes were overexpressed more than fourfold in blood vessels from breast cancer. "The most exciting aspect of this study is that we now have a very large list of potential targets that we will continue to work on for at least the next decade," Klauber-DeMore said. So far, she and her colleagues have only looked at seven out of the 55 potential targets. "This work points us in the direction we need to go to develop the next generation of angiogenesis inhibitors," Klauber-DeMore said. The study was published in the current issue of The American Journal of Pathology. . . . . . . . . . (Medicine.net, Healthday News, By Robert Preidt, [source] May 2, 2008. Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

Thank you, Carole. I know you will let us know what you find. Barbara

Hi Donna and Carole, I searched stats and came up with this one taken in 2004, CDC, and another at NCI (updated 2007). NCI updates every other year - next 2009). http://www.cdc.gov/cancer/lung/statistics/ If anyone has anything more recent it would be appreciated. Call me Mrs. D. Nile, but I'd rather consider Bill a survivor as among the percentage who will live longer. After all, newer treatments are out there which weren't out there in 2004, when Bill was first diagnosed. Anyway, the stats are not delineated as clearly as we might be able to discern, or maybe it's my lack of expertise in reading statistical data. What I know of stats (one university course in Sociology), the collecting of data depends highly on the population under study, and reaching all those who are relevant to the subject being studied. There are many variables (age, stage, general health prior to diagnosis, stamina, etc.) - so, I always consider stats with that in mind. As has been noted by Disraeli and Twain, "There are lies, damned lies, and statistics." Barbara

CONGRATULATIONS! What beautiful news, Dana. Many blessings wished, Barbara

Hello Marie, A very warm welcome to you. So glad you have found this site. I am sure you will find some of your old friends, and many new ones, as well. Barbara

Please accept my condolences on the loss of your friend, Heather Saler ("Hebbie"). As a reader of Heather's inspirational efforts in the walks and fundraisers for lung cancer research over the years, I am deeply saddened at your and our loss. Barbara

http://www.news-medical.net/?id=38194 ARTICLE: . . . . . . . . . Scientists at the IFOM-IEO Campus have revealed the function of a protein that is indispensable for passing on an accurate copy of the genome from mother to daughter cells. This study, published in Cell, opens up new avenues of research to reduce the toxicity of chemotherapy in the treatment of cancer. The protein can be compared to a cowboy's lasso: it catches chromosomes and ties them to a transitory structure assembled during cell division. Once they have been neatly tied up, the chromosomes await the end of replication to be equally distributed between the two daughter cells. But if the lasso doesn't catch them, chromosomes end up being randomly scattered, with potentially disastrous genetic effects: should cells survive this, they receive the wrong genetic inheritance, with dire consequences. The structure and function of this chromosomal lasso were discovered in Milan, at the IFOM-IEO Campus (that hosts the laboratories of the FIRC Institute of Molecular Oncology Foundation - IFOM - and of the European Institute of Oncology - IEO) and these findings have just been published in the prestigious scientific journal, Cell. "We've been studying a molecule called Ndc80 - explains Andrea Musacchio, principal author of the study, and head of a research group in the Department of Experimental Oncology (IEO). This protein is a key player necessary for the correct distribution of genetic inheritance. Ndc80 could potentially be used as a target for new drugs that would have fewer toxic side-effects than current drugs, such as paclitaxel (originally called taxol), which mainly act as inhibitors of cell replication." The operative word here is 'mainly'. Although many drugs used in traditional chemotherapy act on molecular targets that are in involved in the duplication of cells (during a phase known as 'mitosis'), these targets also have other cellular functions. Ndc80, on the other hand, performs its job only during mitosis. So, by blocking Ndc80, the only cells that would be affected would be the dividing ones. Any other cells would be unaffected. Musacchio and his colleagues (together with co-author Peter De Wulf and his research team) are already testing a number of substances that might be able to block the action of Ndc80. The published findings were a truly international effort involving research groups from England and the USA; much of the work was made possible thanks to financial support from the Italian Association for Cancer Research (AIRC). "We've been studying the mechanisms that regulate accurate genome duplication for many years now - explains Musacchio. Our hope is to discover new, less toxic drugs for chemotherapy. Cancer cells grow at a much faster rate than normal cells and traditional chemotherapy drugs, like paclitaxel, block this cell division process. The efficacy of these drugs depends on differences in the growth rates of normal and cancer cells. This means that paclitaxel is toxic for all cells undergoing mitosis; however, since most mitotic cells in cancer patients are actually cancer cells, it follows that this drug will do most of its damage in cancer cells. The problem is that paclitaxel acts on proteins that are essential not only for cells to divide, but also for other phases of the cell cycle. This means that the drug has significant associated toxicity, something we would rather avoid. We had hypothesized that Ndc80 was only active during cell division, which is why we thought it might be an interesting target to study. And our results proved us right. We discovered that Ndc80 acts as a kind of molecular lasso that tethers chromosomes to the mitotic spindle, a molecular structure that only forms during mitosis. Ndc80 straps chromosomes firmly onto the spindle until the dividing cells separate; after this stage, it is of no more use to the cell. So, if we interfere with Ndc80, we can significantly reduce the so-called 'toxicity window'." Any drug that inhibits the function of Ndc80 would therefore be much more tumor-specific than currently available treatments. "Peter De Wulf and I - continues Musacchio - have already flagged some interesting molecules. Our in vitro work now needs to be validated in vivo, first in laboratory models, and then in standard clinical trials." Musacchio and colleagues have made an important step forward in understanding the molecular workings of normal and cancer cells. This work is the starting point for the development of new drugs. But, as this scientist points out, the expertise needed to achieve this latter step is sorely lacking in Italian academic research environments. "The development of new drugs - explains Musacchio - depends on the mutual interaction of Chemists and Biologists. Italian academic research still hasn't capitalized on this, and academia limits itself to the identification of therapeutic targets. While this is a necessary and important step, the development of new drugs is left in the hands of the large pharmaceutical companies." This situation is unacceptable. Italian academic research (which is, by definition free, and not profit-led) can - and should - also focus on screening for molecules that can interact with newly-identified targets to inhibit them. To add insult to injury, such compounds are often neglected by pharmaceutical companies, when they do not fall within their production strategies. Musacchio and De Wulf's strategy in their hunt for molecules that can inhibit Ndc80, exemplifies what needs to be done. But, unfortunately, their approach is not commonly adopted in Italy, and the gap between basic and translational or applied research grows ever wider. Musacchio uses a vivid metaphor to describe the situation: "We discover mountains to climb, but we don't have the equipment needed to guarantee the success of our expeditions". We shouldn't underestimate the value of the collections of compounds hidden away in academic chemistry laboratories; these could be made publicly available. Mussacchio concludes: "A contribution of this kind would be invaluable for international research and a crowning achievement for our Nation". The findings are the result of a collaborative effort between the IFOM-IEO Campus and the University of North Carolina (USA), Colorado State University (USA), the Sir William Dunn School of Pathology (UK), the Wellcome Trust Centre for Cell Biology at the University of Edinburgh (UK) and the University of London (UK). The research was funded not only by AIRC, but also by the International Association for Cancer Research, the Telethon Foundation and the Italian Ministry of Health. . . . . . . . . . (News-Medical.net, Source: Research at IFOM-IEO Campus, May 8, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

Hi Gail, I just saw your post. I am sorry that Hank is still having the s.o.b. issues. My thoughts are that seeking out the pulmonologist may lead to a solution. Hopefully, Wednesday may bring Hank and you something good toward resolving that. Keeping you in thoughts, Barbara

http://www.cancernews.com/data/Article/606.asp ARTICLE: . . . . . . . . . By activating a cancer suppressor gene, a small molecule called nutlin-3a can block cancer cell division, according to researchers at the National Cancer Institute (NCI), part of the National Institutes of Health. This activation of the p53 gene leads to cellular senescence, a process by which cells lose their ability to grow and divide. An opportunity for new genetic mutations occurs each time a cell divides, so limiting the number of cell divisions in a cancer cell inhibits tumor progression. This study is published in the May 1, 2008, issue of Cancer Research. Activation of p53 can suppress tumor growth through more than one mechanism. It can interfere with the cell cycle, prompting a cell with unrepaired DNA damage to commit suicide through a complex signaling pathway called apoptosis. Alternatively, p53 may trigger cellular senescence in response to DNA damage or cellular stress. The expression of p53 is regulated by Mdm2, a protein that is overexpressed in several human cancers. Nutlins are small-molecule inhibitors that prevent the p53 protein from forming a complex with Mdm2, resulting in activation of p53. Previous studies have shown that nutlin can induce apoptosis in human cancer cells. "Although p53 is mutated or deleted in about half of all cancers, it is still potentially functional in the other 50 percent," said Curtis C. Harris, M.D., chief of the Laboratory of Human Carcinogenesis at NCI's Center for Cancer Research and an author of the study. "A better understanding of molecules, such as nutlin-3a, that can activate p53 may lead to the development of new treatment options for certain cancers." To examine the effects of nutlin-3a on cellular senescence, the Harris team exposed human skin cells and cancer cells to two different forms of nutlin-3: forms a and b. (Nutlin-3a has a 150-fold greater affinity for Mdm2 than nutlin-3b.) After a seven-day exposure period, the scientists found that almost 100 percent of the cells treated with nutlin-3a had stopped proliferating. These cells did not regain the ability to proliferate even after being removed from nutlin-3a, indicating that they had undergone permanent senescence. By contrast, nutlin-3b had little effect on the cells. Next, the researchers investigated whether the senescence induced by nutlin-3a is dependent on the presence of p53 protein. After exposure to nutlin-3a for seven or 14 days, more than 80 percent of the human cells containing a functional p53 gene exhibited signs of senescence. The researchers also found that nutlin-3 treatment increased the expression of p53. However, the researchers did not observe any changes in p53-deficient cells. Previous research by this team showed that the genes affected by p53 activation differed depending on the type of activator. To gain a better understanding of nutlin-3a-induced senescence, the researchers used microarray analysis to determine the effect of p53 activation on gene expression after cancer cells were treated with nutlin-3a. Microarray analysis is a technique that allows researchers to examine the expression of thousand of genes simultaneously. Almost 3,000 genes were differentially expressed when cells with normal p53, cells with mutant p53, and p53-deficient cells were compared. Among the genes with increased expression after nutlin-3a-activation of p53 were several genes that play a role in cellular senescence and cell death. The researchers also found that the inhibitor of growth 2 gene (ING2) was among those with decreased expression in response to nutlin-3a treatment. ING2 regulates gene activation or expression, and it may play a role in tumor development, cell proliferation, and senescence. The researchers found that p53 seemed to suppress ING2 expression by binding directly to two sites on the ING2 promoter. "This study further characterizes the actions of nutlin-3a on genes that can play a role in the development of cancer," said Harris. "Our study reinforces the idea that using Mdm2 inhibitors, such as nutlin-3a, to promote the growth suppressive and cell-killing activity of p53 is a potentially valuable strategy to pursue in cancer treatment." . . . . . . . . . (Cancer News, Source: National Cancer Institue, May 1, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

http://tinyurl.com/48kze8 ARTICLE: . . . . . . . . . A recently published study finds that results from positron emission tomography (PET) scans often influence a physician’s intended management plan among elderly patients diagnosed with cancer. Full details of the study were published in the Journal of Clinical Oncology. Many types of testing are involved in the diagnosis and evaluation of cancer as well as measuring its response to treatment. In some cases PET scans may be used to evaluate changes in cancerous cells that are often undetectable by X-ray or computed tomography (CT) scans. A PET scan receives its images by administering a radioactive substance to the patient that is then taken up by the cancer cells, allowing the radiologist to visualize areas of increase activity. A CT scan uses special X-ray equipment to provide cross-section pictures of organs and tissues of the body. In some situations these PET and CT may be combined for increased sensitivity. Currently, Medicare covers PET and CT scans if there is sufficient data on the patient’s cancer diagnosis to justify these tests. The National Oncologic PET registry (NOPR) ensures that this information is gathered and assesses how PET scans affect treatment decisions. In the current study, the NOPR collected questionnaires from physicians regarding intended treatment plans for elderly patients diagnosed with cancer, before and after PET scanning. Conducted over a period of one year, 22,795 studies were collected from 1,178 medical centers within the United States. PET/CT scans were performed equally for the purpose of diagnosis, initial cancer staging, restaging after treatment, and to evaluate suspected cancer recurrence. Pancreatic, prostate, and ovarian cancer represented approximately 30% of the total cases. Results of the study revealed that had PET scan results not been available, the physician would have chosen other imaging options. PET scans appeared influential in treatment planning: after receiving PET scan results, treatment plans were changed to observation in 37% of cases and treatment was altered in 48% of cases. Among patients with planned biopsies prior to PET scans, biopsy was avoided in 70% of cases. If the pre-PET management plan included treatment, the post-PET plan involved a major change in type of treatment among 8.7% patients and a goal change in 5.6%. Further analysis revealed that post-PET plans were three times more likely to lead physicians to treat patients rather than postpone treatment (28.3% versus 8.2%). Overall results indicated that physicians changed their intended treatment plans in 36.5% of cases following PET scans. Researchers concluded that PET scans frequently influence treatment strategies for elderly patients diagnosed with cancer. . . . . . . . . . (CancerConsultants.com, Oncology Resource Center, May 8, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

http://www.sciencedaily.com/releases/20 ... 115829.htm ARTICLE: . . . . . . . . . Researchers at the OU Cancer Institute have identified a new gene that causes cancer. The ground-breaking research appears April 28 in Nature’s cancer journal Oncogene. The gene and its protein, both called RBM3, are vital for cell division in normal cells. In cancers, low oxygen levels in the tumors cause the amount of this protein to go up dramatically. This causes cancer cells to divide uncontrollably, leading to increased tumor formation. Researchers used new powerful technology to genetically “silence” the protein and reduce the level of RBM3 in cancerous cells. The approach stopped cancer from growing and led to cell death. The new technique has been tested successfully on several types of cancers – breast, pancreas, colon, lung, ovarian and prostate. “We are excited about this discovery because most cancers are thought to come from mutations in genes, and our studies, for the first time, have shown that too much of this type of protein actually causes normal cells to turn into cancer cells,” said Shrikant Anant, Ph.D., a cancer biologist at the OU Cancer Institute and principal investigator on the project. Anant said they found RBM3 protein in every stage of many cancers, and the amount of protein increased as the cancer grew. The protein helped the cancer grow faster, avoid cell death and was part of the process that formed new blood vessels to feed the tumor. “This process, called angiogenesis, is essential for tumor growth and suggests that targeting RBM3 may be an extremely powerful tool against many and perhaps all solid tumors,” Anant said. A quarter of the funding for the cancer research comes from an $800,000 grant from the National Institutes of Health with remaining funds from the University of Oklahoma College of Medicine. The next step for Anant, Dr. Courtney Houchen and their research team at the OU Health Sciences Center is to develop agents that block the protein function in a variety of cancers. Researchers expect to start clinical trials at OU in about five years. . . . . . . . . . (Science Daily, Research News, Source: Oklahoma University Cancer Institute, May 9, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

http://www.newswise.com/articles/view/540461/?sc=dwhn ARTICLE: . . . . . . . . . Newswise — Viruses are masters of deception, duping their host's cells into helping them grow and spread. A new study has found that human cytomegalovirus (HCMV) can mimic a common regulatory protein to hijack normal cell growth machinery, disrupting a cell's primary anti-cancer mechanism. Writing in the May 9 issue of Science, researchers from the University of Wisconsin-Madison and Harvard Medical School report that a viral protein, called UL97, masquerades as a normal regulatory enzyme to modify a tumor-suppressing protein in human cells. Unlike the normal enzyme, which can be switched on and off by the cell as needed, the viral stand-in lacks an off switch and evades cellular control. The findings represent a previously unknown way that viruses can cause uncontrolled cell growth and division. Cells normally have tight regulatory mechanisms in place to limit multiplication to appropriate situations, such as replacing worn-out cells or repairing damage. Uncontrolled cell proliferation can lead to cancer and other disorders. One of the most important cellular control mechanisms works through a protein called the retinoblastoma tumor suppressor protein, which slows cell growth. "The retinoblastoma pathway is like the brakes on a car. It prevents tumor cells from growing out of control," says Robert Kalejta, an assistant professor in the UW-Madison Institute for Molecular Virology and McArdle Laboratory for Cancer Research, who led the new study. "This pathway is mutated in essentially all human cancers." Disrupting this pathway is also advantageous for viruses. Unable to reproduce on their own, viruses rely on co-opting their host's cellular machinery, like an occupying army taking over a local factory. They are especially good at overriding or bypassing built-in control mechanisms, Kalejta says. "Viruses are well known to encode proteins that have similar activities to cellular proteins, but they're just different enough that they're beneficial to the virus," he says. "[uL97] shares the same activities as the cellular protein, but it lacks all of the control mechanisms." In essence, UL97 disables the brakes and hits the gas. Once a host cell is primed toward growth, HCMV takes over and steals the cell's machinery to reproduce itself. The virus's bloodhound-like ability to seek out and target the most essential pieces of a cell's machinery makes it a valuable research tool, Kalejta says. "Viruses are smarter than we are. They know a lot more about cells than we do, because their life depends on it - they're obligate intracellular parasites," he says. "If they attack a part of the cell - a process or a protein - you know it's important for the cell. If the virus pays attention to it, you should too." Kalejta next hopes to use UL97 to find other proteins that may be important for cell growth. He also sees potential clinical applications down the road. HCMV infection is very common and, though it remains asymptomatic in most people, it has been implicated in some cancers and can cause trouble in people with compromised or suppressed immune systems, such as AIDS patients and transplant recipients. In addition, UL97-like proteins are also found in the other seven human herpes viruses, some of which are directly linked to cancers. The advantages of the research are two-fold, Kalejta says. "We're studying a virus that causes human disease and might eventually find a way to treat that infection and help patients. At the same time, we're learning about how the cell works, which has implications for patients that don't have infections," he says. "You get two for the price of one." Other authors on the paper include Adam Hume, Jonathan Finkel, and Michael Culbertson from UW-Madison and Jeremy Kamil and Donald Coen from Harvard Medical School. The work was funded by grants from the National Institutes of Health, the Wisconsin Partnership for a Healthy Future, the Burroughs Wellcome Fund, and the American Heart Association. . . . . . . . . . (NewsWise, Medical News, Source: University of Wisconsin-Madison, May 8, 2008) Disclaimer: The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.