Women With Dense Breasts or a Family History of Breast Cancer May Want to Consider Screening in Their 40s
WebMD Health News
Reviewed by Louise Chang, MD
April 30, 2012 -- A pair of new studies aims to clear up some of the confusion over what age women should start getting routine mammograms to screen for breast cancer.
The studies, which are published in the Annals of Internal Medicine, show that a woman in her 40s who has extremely dense breasts, or who has a mother or sister with breast cancer, reaps the same benefits and drawbacks from getting regular mammograms as a woman in her 50s.
Researchers say that meets a "threshold of risk" that may help guide women and their doctors to start regular mammograms at age 40 instead of age 50, as some current guidelines suggest.
"They're really taking a better look and saying if you have risk factors, you should be screening at age 40 because then the benefit is there," says Stephanie Bernik, MD, chief of surgical oncology at Lenox Hill Hospital in New York City.
Bernik says she was relieved to see the new studies because she felt guidelines issued in 2009 that recommended that most women wait until age 50 to start getting regular mammograms were premature and might discourage some younger women who could benefit from the tests.
"This is better than what they said before," says Bernick, who was not involved in the research.
But for some researchers, it's still not enough. Since the research is preliminary and is meant more for policy makers than for individuals, one researcher called it "ivory tower" information that still isn't intended to help a younger woman make a decision.
Refining Recommendations on Mammograms
In 2009, the U.S. Preventive Services Task Force (USPSTF) said that most women should get routine mammograms every two years starting at age 50 instead of age 40.
That recommendation conflicts with guidelines from the American Cancer Society, the National Cancer Institute, and the American College of Radiology, which all recommend screening starting at age 40. And it has drawn mixed reactions from patients and doctors.
Some groups applauded the conservative approach, saying that it would reduce the harms of over-testing and overtreatment, which are greatest for women in their 40s.
Others said it would unnecessarily put women's lives at risk, since cancers found in younger women can be aggressive and early detection of an aggressive cancer may be a woman's best hope for survival.
Ultimately, the USPSTF said the decision to start breast cancer screening before age 50 should be left up to individual women and their doctors.
But until now, there's been little information to help guide that decision.
Family History or Dense Breast Tissue Doubles Risk
The new studies, which were conducted by the same group of researchers that compiled the evidence for the 2009 USPSTF recommendations, are meant to help clarify when mammograms might be useful for younger women.
The first study used four different models to simulate the benefits and harms of screening mammography in women ages 40 to 49.
That study found that women in their 40s need to have double the average risk of getting breast cancer to get the same degree of benefit from regular mammograms, meaning every other year,as women in their 50s.
"Between 40 to 49, the chance of developing breast cancer is under 2%, so even when you double that, it's still low," says researcher Jeanne S. Mandelblatt, MD, MPH, associate director for population sciences at Georgetown University Medical Center's Lombardi Comprehensive Cancer Center in Washington, D.C.
In a companion study, researchers asked what risk factors might actually double a woman's risk for breast cancer in her 40s.
For that study, researchers reanalyzed data from 66 published studies and included data on more than 380,000 women who are being tracked through the Breast Cancer Surveillance Consortium, a network of seven mammography registries.
Out of 13 distinct risk factors identified through the studies and registries, only two fully doubled a woman's risk for breast cancer in her 40s.
"To have a twofold increase in risk, you need to have a first-degree relative -- a mother, daughter, or sister -- with breast cancer. Or you need to have extremely dense breasts. There aren't that many women who have either of those conditions," Mandelblatt says.
For women with more than one first-degree relative with breast cancer, the risks were even higher -- four to 12 times greater than average.
If a first-degree relative was diagnosed before age 40, a woman's risk of breast cancer was three times higher than average.
The issue of breast density is a complicated one, researchers admit, because density can only be determined by first getting a mammogram.
Experts don't recommend that women get a baseline mammogram to discover breast density.
"Mammography density is sort of a newer area," says researcher Heidi D. Nelson, MD, MPH, an investigator at the Oregon Evidence-based Practice Center and the Knight Cancer Institute at Oregon Health & Science University in Portland.
"Radiologists aren't in good agreement about how to read breast density, and we're not sure how to drive that car, yet, really," Nelson says. "So it would be good to maybe wait for more research about exactly how to make decisions with that information."
But Nelson says the study should also comfort women who worry that things like physical inactivity and body weight might put them at increased risk for breast cancer. The study found those had relatively little influence on a person's risk. Other factors that didn't appear to raise risk substantially included race, smoking, and alcohol use.
"What's really reassuring is that there are a lot of risk factors that really don't have a huge increase in risk attached to them," says Nelson.
Understanding Personal Risk
Researchers were also careful to stress that the pair of studies was meant for policy makers, not for individual women to use to try to discern their own risk.
"These data do not present recommendations on what women should or shouldn't do," says Diana Buist, PhD, a senior investigator at Group Health Center for Health Studies in Portland, Ore.
"This should not be used for adding your risk as an individual person," Buist says, adding that it's better to talk through issues of risk with your doctor before deciding on whether to get a mammogram.
"Mammography is not a perfect tool," Buist says. "It just doesn't work as well in younger women. Because it doesn't work as well, it means that there are harms and benefits that are important for women to understand."
Other experts found the studies frustrating because they stopped short of offering any new advice.
"I'm not sure where that leaves women in their 40s who aren't sure what to do," says Kathryn Evers, MD, director of mammography at Fox Chase Cancer Center in Philadelphia. "I think the people who know they have bad family histories know they want mammograms, and it's not a discussion. I think for everybody else it's a very difficult problem."
"Most women who get breast cancer don't have these risk factors. What do you do if you're a 45-year-old woman with kids and you're scared?" Evers says. "It is ivory tower research in a lot of ways, and it's very hard to get a good practical message out of it, for me."
Advice to Women Considering Mammograms
Until there are better screening tools to replace mammography, Evers say there are two things women can do to better use the test.
The first is to find a good doctor who will carefully discuss the benefits and risks.
Drawbacks of mammography include false-positive results, radiation exposure, false reassurance, pain, over-diagnosis -- meaning the diagnosis of a tumor that isn't necessarily dangerous -- and overtreatment.
Studies show that about half of women who get an annual mammogram for 10 years starting at age 40 will have at least one false-positive result that leads to a cancer scare.
The benefits of mammography include early detection. One review suggests that mammograms have reduced breast cancer deaths by 15%.
If you do decide to get tested, Evers says it's smart to seek out a radiologist who is a dedicated mammographer, which means that they only read mammograms.
Mammographers are specialists, and studies show they are more likely to catch cancer when it's there and correctly rule it out if it's not. They're also less likely to order unnecessarily follow-up tests.
Van Ravensteyn, N. Annals of Internal Medicine, April 30, 2012. Nelson, H. Annals of Internal Medicine, April 30, 2012. Brawley, O. Annals of Internal Medicine, April 30, 2012. News release, Annals of Internal Medicine. Stephanie Bernik, MD, chief of surgical oncology, Lenox Hill Hospital, New York. Jeanne S. Mandelblatt, MD, MPH, associate director for population sciences, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, D.C. Heidi D, Nelson, MD, MPH, investigator, Oregon Evidence-based Practice Center and the Knight Cancer Institute, Oregon Health & Science University, Portland. Diana Buist, PhD, senior investigator, Group Health Center for Health Studies, Portland, Ore. Kathryn Evers, MD, director of mammography, Fox Chase Cancer Center, Philadelphia, Pa.
Dear ISCA, How do I go about thanking you for giving me back my life! There are no words that can adequately express how I feel. When my conventional oncologist told me I had stage III breast cancer and that I had no options, besides surgery, chemo and radiation, I felt that I would be going down a dark deep hole that I could never climb out of. Dr. Orn gave me hope, calmed all my fears and helped put me back in control of what was happening in my body. He told me it was up to me to follow a change in lifestyle and diet and by doing that and allowing me to be a part of the trial taking place in the Bahamas, I have been able to rid my body of the cancer 100%. When Dr. Lunn told me that it was up to me to make my immune system strong by exercise, supplements and diet and how well it worked would depend on me, I knew that I would be in control. With ISCA as my backup support all along the way, together we made it work. I began as a hysterical woman with no hope and have come out of this entire journey as a much more positive person. Along the journey, following the strict protocol, I have also lost 70 pounds, a feat that was a pleasant side effect that I had been trying to do for the last 30 years. I tell everyone I meet about ISCA and the difference it has made in my life. Whenever I had a question or a doubt along the journey, you were always there to give me the support I needed. I was only an email or phone call away. You told me how stress was a huge enemy of mine, which causes illness in all of us. Therefore, I thank God everyday for leading me to ISCA, which saved my life. Someday I would like to meet you in person, Dr. Orn, and give you a big hug to say thank you. Although I must admit Skype is the next best thing! Today, I am back to my career, but this time with a much healthier way of approaching life. I try not to let things cause me stress and if they do, I let them go, but I keep my newly found lifestyle changes of diet and exercise. They are a part of the "new me". I know that I can never let up, or I could end up in the same boat again. So thanks to Dr. Orn and ISCA, my whole approach to life has been changed for the better!
Thank you from the bottom of my heart
Diabetes drug metformin may prevent cancer By Aaron Derfel, Postmedia News January 19, 2012 MONTREAL - The most widely prescribed drug to treat Type 2 diabetes might also help prevent colon cancer in those who are considered at high risk, suggests new research carried out by a team of Montreal scientists.
Metformin has already been shown in previous studies to cut cancer rates by 40 per cent in those taking the medication, compared with diabetics who are not.
Researchers at McGill University and the Universite de Montreal sought to understand exactly how Metformin might prevent cancer. The prevailing theory before their lab study was that since cancer cells have a voracious appetite for glucose, using a drug to lower glucose levels in the blood for the treatment of Type 2 diabetes might also inadvertently block cancer.
The researchers did confirm that the glucose-lowering action of Metformin does play a subtle role in preventing cancer. But they also made a much more important and unexpected discovery:Metformin protects cells from DNA damage that can lead to cancer.
``Surprisingly, we found that Metformin protected DNA from mutations,'' said the study's director, Dr. Michael Pollak, a professor in McGill's departments of medicine and oncology.
``It is remarkable that Metformin - an inexpensive, off-patent, safe and widely used drug - has several biological actions that may result in reduced cancer risk.''
Cells burn nutrients to produce energy. That burning-off process produces what Pollak likens to a kind of cellular exhaust, known as reactive oxygen species. It's this exhaust that can cause DNA damage inside cells, which in turn can spark cancer.
Metformin acts as a cellular exhaust ``filter,'' Pollak explained, reducing reactive oxygen species.
``The drug seems to selectively prevent (the cellular exhaust) production ... such as those found in cells with oncogenic mutations,'' said study co-author Gerardo Ferbeyre, of U de M's department of biochemistry.
The researchers made the discovery by treating pre-cancerous breast and colon cells with Metformin. The results of their study were published Wednesday in the journal Cancer Prevention Research.
Dear ISCA, Just wanted to express my heartfelt gratitude to you for extending yourself so much on my behalf. To say your extraordinary efforts are so very deeply appreciated is to make the understatement of the year! I am moved to tears that you would help me as much as you have!
Thank you , thank you, thank you from the bottom of my heart and soul!
In the November 1, 2008 issue of The Prostate, researchers at the University of Wisconsin report their finding that a combination of vitamin C and E administered to human prostate cancer cell cultures results in apoptosis (programmed cellular self-destruction). The finding adds support to the hypothesis that vitamin E and selenium are of value in prostate cancer prevention, which is being investigated by the twelve-year Selenium and Vitamin E Chemoprevention Trial (SELECT) of over 32,000 healthy men. For the current study, Nihal Ahmad, PhD and colleagues added varying concentrations of alpha-tocopherol succinate (vitamin E), a form of selenium known as methylselenic acid, or both nutrients to three human prostate cancer cell lines as well as normal prostate epithelial cells. While vitamin E succinate or selenium alone modestly inhibited the growth and viability of prostate cancer cells, the combination of the two dramatically inhibited prostate cancer cell growth while having no effect on either growth or viability of normal cells.
The scientists determined that the nutrients' mechanism involves proteins that are members of the Bcl-2 family, which participate in the control of apoptosis. Apoptosis occurred in all cell lines used in the study, two of which were androgen-insensitive and defective for p53. The finding is important because prostate cancer undergoes a transition from androgen-sensitive to androgen-insensitive disease, and most prostate cancers contain both types of cells.
"We have found that the combination of vitamin E succinate and methylselenic acid was much more effective than either of the agents alone," the authors conclude. "Also, we have used low concentrations of both the agents which makes our finding more relevant to in vivo [living] settings."
Histological slide (H & E stain at x300) showing prostate cancer. On the right is a somewhat normal Gleason Value of 3 (out of 5) with moderately differentiated cancer. On the left is less normal tissue with a Gleason Value of 4 (out of 5) that is highly undifferentiated. The Gleason score is the sum of the two worst areas of the histological slide. (Slide by Otis Brawley) Compound Can Distinguish Between Benign, Localized and Metastatic Prostate Cancer
Researchers have determined that a molecule produced by the body's metabolism could be used to differentiate between benign prostate tissue vs. localized and metastatic prostate cancer. They also found that this molecule, known as sarcosine, may be associated with prostate cancer invasiveness and aggressiveness. The findings were reported by researchers at the Michigan Center for Translational Pathology, Ann Arbor, and were supported by the National Cancer Institute's (NCI) Early Detection Research Network (EDRN). The research appears in the Feb. 12, 2009 issue of Nature. NCI is part of the National Institutes of Health. "Current biomarkers for detection or progression of prostate cancer are not as precise as we would like. Therefore, a more accurate indicator of cancer is of great interest," said Sudhir Srivastava, Ph.D., chief of NCI's Cancer Biomarkers Research Group. "Sarcosine and some other select metabolites may be excellent indicators of cancer progression."
Multiple, complex molecular events characterize cancer development and progression. Determining which molecular networks dictate whether cancer will be confined to the prostate or spread to other parts of the body could lead to the identification of critical biomarkers associated with prostate cancer invasion and aggressiveness.
Although many genes and proteins related to cancer have been extensively characterized by genomic and proteomic studies, little is known about metabolomic changes that mark a tumor's progression. Metabolomics, upon which this current finding is based, is the study of the unique chemical fingerprints that cellular processes leave behind, which can help scientists understand the makeup of a cell. One of the challenges that scientists currently face is integrating genomic, proteomic, and metabolomic information to give a more complete picture of living organisms and the diseases that afflict them.
Using a long-established laboratory technique called mass spectrometry, which sorts chemical compounds by their molecular weight, the researchers profiled more than 1126 metabolites from 262 clinical samples related to prostate cancer (42 tissue samples, 110 urine samples and 110 samples of blood plasma). These metabolomic profiles enabled researchers to distinguish between benign prostate tissue, clinically localized prostate cancer, and metastatic disease. Sixty metabolites were identified in localized and/or metastatic prostate tumors that were not present in benign prostate tissue. Ultimately, six metabolites, including sarcosine, were found to be significantly elevated during progression from benign tissue to localized cancer to metastatic disease. Sarcosine was also detected in the urine of men with prostate cancer. Because this metabolite showed progressive elevation from benign tissue to localized prostate cancer to metastatic disease, it was selected for further study.
To investigate the role of sarcosine in prostate cancer progression, the researchers performed analyses of laboratory-grown cells. They found that sarcosine levels were higher in invasive prostate cancer cells than in benign prostate cells. Moreover, the addition of sarcosine to benign prostate cells caused them to become invasive. By manipulating levels of the enzymes that regulate sarcosine metabolism, the researchers found they were able to control the invasiveness of benign and malignant prostate cells.
"Components of the sarcosine pathway could serve as novel avenues for therapeutic intervention," said Arul M. Chinnaiyan, M.D., Ph.D., Michigan Center for Translational Pathology at the University of Michigan, Ann Arbor. "Our next step will be to confirm these findings in a greater number of specimens and to have our results validated by other laboratories."
Sreekumar A, Poisson LM, Rajendiran TM, Khan AP, Cao Q, Yu J, Laxman B, Mehra R, Lonigro RJ, Yong L, Nyati MK, Ahsan A, Kalyana-Sundaram S, Han B, Cao X, Byun J, Omenn GS, Ghosh D, Pennathur S, Alexander DC, Berger A, Shuster JR, Wei JT, Varambally S, Beecher C, and Chinnaiyan AM. Metabolomic profiles delineate potential role for sarcosine in prostate cancer progression. Nature. February 12, 2009.
The study behind controversial research findings from the US that found a common blood test for prostate cancer has no benefit in reducing deaths has been challenged by Australias and New Zealands peak body for urological surgeons. AUCKLAND, Mar. 24 /Medianet International-AsiaNet/ -- Having carefully reviewed the study into Prostate Specific Antigen (PSA) blood tests undertaken in the United States, the Urological Society of Australia and New Zealand believes that there were design flaws in the US study which invalidate the results. We are concerned that Australian men may be persuaded against having a potentially life-saving PSA blood test following media reports of this US study, said USANZ president, Dr David Malouf.
Dr Malouf, who has just returned from the 24th Annual European Association of Urology Congress in Stockholm, said two studies about the PSA test recently published in the New England Journal of Medicine, one from the US and the other from Europe, had shown very different results and that the conflicting research findings must now be clarified.
The PLCO study in the US involved 76,000 men and did not demonstrate a benefit from screening. USANZ believes there are fundamental flaws in the study design which make the results of this trial less valid. The follow up of patients enrolled in the study was not of adequate duration and in the non-screened or usual care arm of the study more than half of the men underwent PSA testing, thus contaminating the unscreened population Dr Malouf said.
By contrast, the ERSPC study in Europe, commencing in the 1990s and involving 162,000 men in 8 European countries, demonstrated that routine prostate cancer screening could cut death rates from the disease by 20%. The study of men aged between 55 and 69 who underwent screening for prostate cancer had a 20% reduction in the risk of dying from prostate cancer compared with men who were not screened. The trial authors estimated that 1400 men would need to be screened to save one life from prostate cancer. These numbers required to save one life are similar to the numbers in breast and colorectal cancer screening programs. While some commentators have argued that many indolent cancers are unnecessarily detected as part of a screening process, in practice many of these men can be reassured and simply monitored without active treatment in the medium and long term, Dr Malouf said.
Routine population based prostate cancer screening with the PSA blood test is not performed in Australia or New Zealand and is, at present, not advocated by USANZ.
The position of this professional body remains that patients should have access to PSA based testing if they wish, after discussion with their family doctors and/or specialists about the risks and benefits of such testing.
There is firm data that testing reduces the risk of being diagnosed with advanced disease, and that treating prostate cancers following diagnosis can lead to a reduced risk of dying from the disease compared to no treatment.
The findings of the ERSPC study demonstrates the importance of developing new tests to identify aggressive forms of prostate cancer and differentiate them from more slowly growing tumours. Such a test will enable clinicians to focus treatment on men whose cancers pose a threat to their health and avoid over-treatment of men with the more indolent forms of the disease, he said.
Phone: +61 2 9965 9300
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NEW YORK, Apr 08, 2009 (ASCRIBE NEWS via COMTEX) -- A new multi-center study shows that an experimental drug lowers prostate specific antigen (PSA) levels - a marker for tumor growth - in men with advanced prostate cancer for whom traditional treatment options have failed. The study, led by researchers at Memorial Sloan-Kettering Cancer Center (MSKCC), is published today in Science Express, the online version of the journal Science. Most men with metastatic prostate cancer eventually build up resistance to the drugs that lower or block male hormones and develop a more aggressive form of the illness called castration-resistant prostate cancer (CRPC), or hormone-refractory disease. According to the study's findings, investigators studied two novel compounds, RD162 and MDV3100, and not only gained an understanding of their novel mechanism of action, but found that these agents showed activity in CRPC cells in culture and in mice. The study also reports on a Phase 1/2 trial of MDV3100 in 30 patients with advanced CRPC and found that 22 out of 30 men showed declining PSA levels, and 13 out of 30 men (43 percent) had PSA levels fall by more than half.
Several years ago, the senior author of the study, Charles Sawyers, MD, and his colleagues at the University of California, Los Angeles (UCLA), uncovered a potential reason why metastatic prostate cancer patients eventually relapse with CRPC. This insight was used to discover RD162 and MDV3100.
"It's gratifying to know that our hypotheses about why men develop resistance to currently available treatments are confirmed and, most importantly, that there are already patients who are benefiting from our research," said Dr. Sawyers, Chair of the Human Oncology and Pathogenesis Program at MSKCC and a Howard Hughes Medical Institute investigator.
Current treatments for men who have advanced prostate cancers inhibit the activity of male hormones that help drive tumor growth. Many of these drugs disrupt the androgen (male hormone) receptor, which helps regulate cell proliferation, but tumors eventually become resistant to the drugs by expressing higher levels of the receptor. Preclinical studies by Dr. Sawyers and others have demonstrated that CRPC cells have increased expression of the androgen receptor and that overexpression of this receptor may contribute to the progression of disease.
Based on this information, Dr. Sawyers initiated a collaboration with Michael Jung, PhD, Professor of Chemistry at UCLA, that led to the discovery of a number of nonsteroidal, small molecule antiandrogen compounds, including MDV3100, which has been shown to retain its anticancer activity, even when the receptor's expression is elevated.
"The discovery and initial development of this drug was a collaborative effort all done in the academic setting, without reliance on the engine of the pharmaceutical industry that typically drives drug development," said Dr. Sawyers. Dr. Jung's group synthesized the compounds, which Dr. Sawyers' team then evaluated using prostate cancer mouse models engineered to highly express the androgen receptor, mimic progression to castration-resistant disease, and reflect the biology of clinical drug resistance.
According to the new study, the team of researchers tested various compounds to block the androgen receptor in CRPC cells. They chose to further evaluate the drug RD162 and a closely related compound, MDV3100. According to their findings, both drugs inhibit the androgen receptor function by impairing the receptor's ability to enter a CRPC cell's nucleus (called nuclear translocation), blocking it from binding to the DNA of its target genes, and preventing the cell from growing. They found that both compounds worked well in cells in culture, shrank tumors in mice, maintained tumor shrinkage for months, and prevented the androgen receptor from activating additional genes later in the process, or "downstream." Other currently approved drugs cannot disable the receptor in such a way.
The biopharmaceutical company Medivation, Inc., licensed RD162 and MDV3100 from UCLA in 2006 and has already completed enrollment in the first human trial of oral MDV3100 - a Phase 1/2 clinical trial, which was led by investigators at MSKCC and conducted through the Prostate Cancer Clinical Trials Consortium. The Consortium is sponsored by the Department of Defense and the Prostate Cancer Foundation. The trial enrolled men with metastatic, castration-resistant prostate cancer who relapsed after treatment with conventional hormone therapy and demonstrated anti-prostate cancer effects beginning with the first patient treated with MDV3100 at the lowest dose. Further positive results from an additional 110 patients who received the drug at higher doses were recently reported at the ASCO Genitourinary Cancers Symposium in February 2009.
"The declines in PSA levels observed thus far and the general tolerability of this treatment are encouraging," said Howard Scher, MD, a study co-author and Chief of the Genitourinary Oncology Service at MSKCC. "I am looking forward to continuing the study of this drug, which has the potential to be a powerful tool in a limited arsenal of treatments against this deadly form of the disease." A Phase 3 trial is planned to begin later this year.
Researchers at MSKCC, UCLA, Oregon Health and Science University, University of Washington, Seattle, and Medivation, Inc., contributed to the research. Dr. Sawyers and several of the study's authors are co-inventors on patent applications covering RD162, MDV3100, and related compounds.
The study was supported in part by the Prostate Cancer Foundation, the National Cancer Institute, and a Prostate Cancer Research Program Clinical Consortium Award.
April 15, 2009 By ANDREW POLLACK <http://topics.nytimes.com/top/reference/timestopics/people/p/andrew_pollack/index.html?inline=nyt-per> A prostate cancer <http://health.nytimes.com/health/guides/disease/prostate-cancer/overview.html?inline=nyt-classifier> drug developed by the Seattle biotechnology company Dendreon <http://topics.nytimes.com/top/news/business/companies/dendreon-corporation/index.html?inline=nyt-org> prolonged the lives of men in a decisive clinical trial, the company announced Tuesday morning.
The widely anticipated results could pave the way for the drug, called Provenge, to become the first so-called therapeutic cancer “vaccine” to win approval in the United States after numerous failures of such drugs. “This looks like a proof of concept that cancer vaccines can and do work,” said Jeffrey Schlom, an expert on the vaccines at the National Cancer Institute <http://topics.nytimes.com/top/reference/timestopics/organizations/n/national_cancer_institute/index.html?inline=nyt-org> . Such vaccines work by harnessing the patient’s own immune system to fight the cancer. But the success in the trial could revive complaints about the Food and Drug Administration <http://topics.nytimes.com/top/reference/timestopics/organizations/f/food_and_drug_administration/index.html?inline=nyt-org> , which two years declined to approve Provenge despite an endorsement by one of the agency’s advisory committees.
The F.D.A. instead said it wanted more proof that the drug worked and would await results from a trial that was then underway, whose results were announced Tuesday.
The F.D.A.’s decision two years ago ignited an outcry from some prostate cancer patients and from investors in Dendreon, who said the agency was being unreasonable and denying patients a treatment that might work. Tensions ran so high at one point that two prostate cancer specialists, who had urged the F.D.A. not to approve the drug, attended a major conference accompanied by bodyguards, saying they had been threatened.
“Since that delay we have lost a lot of good men,” Ted Girgus of Bellingham, Wash., who has advanced prostate cancer, said Tuesday, calling the F.D.A. decision “a punch in the stomach.” Mr. Girgus, 65, who also owns Dendreon stock, said patients like himself are “looking into the abyss.”
“We know what our prognosis is,” he said. “But we want a chance.”
Dendreon did not reveal the actual results of its trial, saying they would be presented at a urology meeting on April 28.
But Mitchell Gold, the company’s chief executive, told analysts on a conference call, “It was an unambiguous hit on the primary endpoint of overall survival.” He said the outcome met the goals the company and the F.D.A. had agreed upon and that the results were consistent with those seen in earlier trials of Provenge.
In an interview Dr. Gold said Provenge would have had to reduce the risk of death by 22 percent compared to a placebo to meet the F.D.A. requirements for statistical significance.
Dendreon’s stock soared on the news. The shares were up more than 130 percent for the day, closing at $16.99.
The stock, which closed Monday at $7.30, had nearly tripled from its 52-week low of $2.55 in early March on anticipation of positive results. But there were also many investors who shorted the stock, betting the drug would fail in the clinical trial.
The trial involved 512 patients whose cancer had spread beyond the prostate gland and who were no longer benefiting from therapies intended to deprive the tumors <http://health.nytimes.com/health/guides/disease/tumor/overview.html?inline=nyt-classifier> of testosterone <http://health.nytimes.com/health/guides/test/testosterone/overview.html?inline=nyt-classifier> .
Dr. Gold said there were about 100,000 men who get such a diagnosis each year. The only approved treatment for them now is the Sanofi-Aventis <http://topics.nytimes.com/top/news/business/companies/sanofi_aventis/index.html?inline=nyt-org> chemotherapy <http://topics.nytimes.com/top/news/health/diseasesconditionsandhealthtopics/chemotherapy/index.html?inline=nyt-classifier> drug Taxotere, which extended median survival by about 3 months in trials.
Mark Monane, an analyst at Needham & Company, said sales of Provenge might reach $500 million to $1 billion a year.
Therapeutic vaccines like Provenge do not aim to prevent the disease, as a childhood vaccine does. Rather they aim to train the body’s immune system to attack the cancer once the patient is already ill.
There is already an approved treatment for bladder cancer <http://health.nytimes.com/health/guides/disease/bladder-cancer/overview.html?inline=nyt-classifier> that stimulates the immune system in general, but not specifically to fight the cancer. The cervical cancer vaccine <http://topics.nytimes.com/top/news/health/diseasesconditionsandhealthtopics/cervicalcancervaccine/index.htm?inline=nyt-classifier> now in use, Gardasil, is a more traditional preventive vaccine that works because cervical cancer <http://health.nytimes.com/health/guides/disease/cervical-cancer/overview.html?inline=nyt-classifier> is caused by a virus.
Proponents say cancer vaccines, also known as immunotherapy, could be a more precise way to attack cancer than bombarding them with poisons, as is now down in chemotherapy.
But development of cancer vaccines has been a path marked by numerous failures until now. Indeed, another prostate cancer vaccine called GVAX, developed by Cell Genesys <http://topics.nytimes.com/top/news/business/companies/cell-genesys-inc/index.html?inline=nyt-org> , failed in late-stage clinical trials last year.
Provenge had become a symbol of the sometimes passionate debate between patients who want faster access to experimental drugs and those who believe society as a whole benefits from greater proof that drugs work.
In an earlier trial, men who received Provenge lived a median of 25.9 months, compared with 21.4 months for those who received a placebo. At the end of three years, 34 percent of the men who got Provenge were alive, compared to only 11 percent for those who received a placebo.
Based on those results, an advisory panel to the F.D.A., meeting in March 2007, voted 13 to 4 that there was “substantial evidence” that the drug worked, and 17-0 that the drug was safe.
Still, some members of the committee said the evidence was somewhat weak because that trial involved only 127 men. And it had been intended to measure something different — not whether Provenge prolonged life, but whether it delayed the worsening of cancer. And the drug failed to do that by a statistically significant measure.
Two months later, the F.D.A. declined to approve Provenge, saying that more data were needed.
Protestors rallied outside an F.D.A. office in Rockville, Md., in September 2007. They took out ads in newspapers and on buses in the Washington area, including one that said “The FDA: killing hope, shortening lives.”
A group called Care to Live sued the F.D.A. to try to reverse the decision. But the courts essentially threw out the lawsuit, saying the F.D.A. had not made a final decision that could be challenged.
Harsh criticism was also directed against two prostate cancer specialists who had voted against Provenge on the advisory committee and later wrote letters to the F.D.A. urging that the drug not be approved. The two doctors, Howard I. Scher of Memorial Sloan-Kettering Cancer Center <http://topics.nytimes.com/top/reference/timestopics/organizations/m/memorial_sloankettering_cancer_center/index.html?inline=nyt-org> and Maha Hussain of the University of Michigan <http://topics.nytimes.com/top/reference/timestopics/organizations/u/university_of_michigan/index.html?inline=nyt-org> , were accompanied by bodyguards when they attended the nation’s largest cancer medical meeting in 2007.
Still, many prostate cancer patient advocacy groups did not support all those tactics or the lawsuit.
“I think the stockholders were more angry than the prostate cancer community,” said Jim O’Hara, a prostate cancer survivor and help line facilitator for the Prostate Cancer Research Institute, a patient education group. “The majority of the community that I talk to wants to see something approved that has gone through legitimate tests.”
Since the F.D.A. declined to approve Provenge, prostate cancer drugs from Cell Genesys, Novacea <http://topics.nytimes.com/top/news/business/companies/novacea-inc/index.html?inline=nyt-org> and GPC Biotech have failed in clinical trials.
Patients treated with Provenge have some white blood cells removed. Dendreon mixes those white cells, which are part of the immune system, with a genetically engineered protein that is a combination of an immune system stimulator and a molecule found in prostate cancer cells but only rarely elsewhere in the body.
The cells are then infused back into the patient, where they are meant to stimulate the immune system to attack anything that looks like the telltale prostate cancer molecule.
The treatment requires three infusions spaced two weeks apart, rather than periodic infusions over the course of months, as is common with chemotherapy. Provenge’s side effects also appear to be milder than those of Taxotere, some doctors say.
“Compared to standard chemotherapy, it’s just a whole lot easier for patients,” said Dr. David Penson, associate professor of urology at the University of Southern California <http://topics.nytimes.com/top/reference/timestopics/organizations/u/university_of_southern_california/index.html?inline=nyt-org> . He was an investigator in the trial and was a consultant to Dendreon a few years ago.
I had the opportunity to be in Chicago at the annual meeting of the American Urological Association (AUA) for the presentation of the Dendreon corporation successful clinical trial results for the first ever prostate cancer vaccine - PROVENGE.
PROVENGE trial results surpassed the survival benefits agreed to by the FDA as necessary for it to be approved as an available treatment. Provenge enhances the patient's own immune system to fight prostate cancer. The first IMMUNOTHERAPY treatment of this type for any cancer; a landmark medical breakthrough.
PHEN has worked with and supported Dendreon over the past few years in the company's quest to gain approval for PPROVENGE. Dr. Mitchell Gold, Dendreon president, presented at PHEN's 2006 African American Prostate Cancer Disparity Summit on Capitol Hill, and he is committed to making certain that Provenge is available to the men who suffer disproportionately from prostate cancer.
Thomas A Farrington PHEN President and Founder
My statement which was presented at the AUA press conference on PROVENGE, Tuesday, April 28th is below. Farrington Statement on Provenge at AUA Statement
Dendreon Provenge Data Release The official release on the Provenge clinical trials results. Provenge Data
Degarelix prostate cancer drug makes testosterone levels fall dramatically and quickly3. December 2008 22:10
Researchers from Canada, the USA, France, Denmark and the Netherlands studied 610 men as part of the Phase Three trial, randomly assigning them to one of three study groups.
"Androgen deprivation hormone therapy is an effective response to prostate cancer, but the drugs that are most widely used cause an initial rise in testosterone - the hormone we are trying to reduce - when the patient first takes them" explains lead author Dr Laurence Klotz from the Division of Urology at the University of Toronto, Canada.
"We prefer to avoid this biochemical surge as it can stimulate the prostate cancer cells and exacerbate a number of clinical symptoms, such as spinal cord compression and bone pain. It could also result in more rapid growth of microscopic disease that is present in the patient but is too small to be detected.
"Degarelix is a new gonadotrophin-releasing hormone (GnRH) antagonist. It works by binding to, and blocking, the GnRH receptors in the pituitary gland, reducing the amount of LH and FSH hormones that are released. This leads directly to a rapid fall in testosterone."
Group one (207 patients) received an injection of 240mg of degarelix in month one, followed by a maintenance dose of 80mg every month for eleven months and group two (202 patients) received 240mg of degarelix in month one followed by a maintenance dose of 160mg for eleven months.
The third group (201 patients) received a monthly 7.5mg dose of leuprolide, which is a GnRH agonist.
At the start of the trial the study participants had a median testosterone level of 3.93 ng/mL. The aim was to reduce this to 0.5ng/mL or less at all monthly measurements from day 28 to day 364.
Eight out of ten study participants completed the trial (504 patients) between February 2006 and October 2007, with similar drop-out and exclusion rates in all three groups.
The key findings were impressive:
- Three days after starting their treatment regimes, 96.1 per cent of the patients on 240/80mg degarelix and 95.5 per cent of the patients on 240/160mg degarelix had achieved a testosterone level of 0.5ng/mL or less. In contrast, median testosterone levels in the leuprolide group had increased by 65 per cent by day three, but had reduced by day 28.
- At the end of the study period, 98.3 per cent of the 240/160mg degarelix group and 97.2 per cent of the 240/80mg degarelix group had achieved a testosterone level of 0.5ng/mL or less. The figure for the leuprolide group was 96.4 per cent.
- PSA levels fell much faster in the degarelix groups when measured at 14 and 28 days - by 64 per cent and 85 per cent in the degarelix 240/80mg group, 65 per cent and 83 per cent in the 240/160mg degarelix group and 18 per cent and 68 per cent in the leuprolide group.
The hormonal side-effects experienced by the three treatment groups were similar to previously reported effects for androgen deprivation hormone therapy.
Patients receiving degarelix were much more likely to experience injection-site reactions than those receiving leuprolide (40 per cent compared to one per cent).
However degarelix patients suffered fewer urinary tract infections than those in the leuprolide group (three per cent versus nine per cent) together with fewer joint pains and chills (four per cent versus nine per cent).
"More than 2,000 patients have now taken part in clinical trials for degarelix and there have been no signs of immediate or late-onset systemic allergic reactions, in contrast to other reported trials of other GnRH antagonists" points out Dr Klotz.
"The aim of the study was to show that degarelix was not inferior to leuprolide when it came to maintaining low testosterone levels over a one-year treatment period. We have conclusively shown that this is the case.
"However, we have also demonstrated that degarelix - which is an antagonist - offers an advantage, in that it reduces testosterone and PSA levels very quickly. It doesn't cause the initial surge of testosterone seen with agonist drugs like leuprolide - the other drug featured in this study.
"This is relevant as biochemical surges in testosterone can stimulate the prostate cancer cells and cause unpleasant side effects for patients. They may also require further drug therapy to counteract the effects of agonist drugs like leuprolide."
New robotic prostate surgery not necessarily better By Julie Steenhuysen Tue Oct 13, 6:41 pm ET
CHICAGO (Reuters) – Men who have less invasive prostate cancer surgery -- often done robotically -- are more likely to be incontinent and have erectile dysfunction than men who have conventional open surgery, U.S. researchers said on Tuesday.
Many men, especially those who are wealthy and highly educated, favor minimally invasive surgery because they assume the high-tech approach will yield better results, but the evidence on that is mixed, the team reported in the Journal of the American Medical Association.
"We found men undergoing minimally invasive versus open surgery were more likely to have a diagnosis of incontinence and erectile dysfunction," Dr. Jim Hu of Brigham and Women's Hospital in Boston said in a telephone briefing. Hu said use of minimally invasive surgery has taken off since the introduction and heavy marketing of robot-assisted surgery, such as the da Vinci system made by Intuitive Surgical Inc.
The system consists of robotic arms, controlled from a console, that allow surgeons to perform less invasive surgeries. Hospitals advertise the systems as being able to reduce trauma, blood loss, risk of infection, scarring and often pain.
Hu said so far, there have been few studies that compare minimally invasive surgery with open surgery.
To do that, he and colleagues used billing data from the Medicare insurance program for the elderly on procedures done from 2003 to 2007. During that time, use of minimally invasive surgery for prostate cancer increased fivefold.
While both approaches fared equally well as a cancer treatment, they found that men who got the minimally invasive approach had shorter hospital stays, were less likely to need blood transfusions, and had fewer breathing problems after surgery than those who got conventional surgery.
But they were also more likely to have complications involving the genital and urinary organs, and they were more often diagnosed as having incontinence and erectile dysfunction than men who got open surgery.
The researchers also noted that fewer black and Hispanic men had the minimally invasive surgery, while Asians were much more likely to get the high-tech surgery.
CHOICE RELATED TO EDUCATION, WEALTH
Men who got the minimally invasive surgery were far more likely to live in areas with at least 90 percent high school graduation rates and median income of at least $60,000.
The fact that highly educated, wealthier men favored the higher technology alternative "despite insufficient data demonstrating superiority" may reflect a healthcare system "enamored with new technology" that increases health costs without offering clear benefits, Hu and colleagues wrote.
Ryan Rhodes, marketing director for Intuitive Surgical, disputed the findings.
"There have been over 800 papers published in peer reviewed journals talking about the outcomes of radical prostatectomy. The majority of these were favorable," Rhodes said.
He said the current study used Medicare billing data, which does not distinguish between robot-assisted and other types of minimally invasive prostate surgery.
"Looking at the data, you cannot accurately assess which patients were operated on robotically," he said.
Dr. Herbert Lepor of New York University's Langone Medical Center analyzed several studies on robotic-assisted prostate surgery in a paper published this year in Reviews in Urology. He said so far the evidence does not suggest the robotic procedure is superior to open surgery.
Lepor, who was not involved in the study, estimates that about 80 percent of minimally invasive prostate cancer surgery is done robotically. "What drives this is the industry creating the need," he said.
"We've increased the cost of care with the robot," he said. "Now what we are learning is continence and potency seem to be inferior."
WASHINGTON — Many hospital patients are dissatisfied with some aspects of their care and might not recommend their hospitals to friends and relatives, the federal government said Friday as it issued ratings for most of the nation’s hospitals, based on the first uniform national survey of patients. For complete story, click here.
Tuesday, 03 February 2009 00:00 Response Genetics, Inc. RGDX, a company focused on the development and sale of molecular diagnostic tests for cancer, announced today it has signed a nonexclusive license with Roche Diagnostics for the use of Response Genetics’ patented PCR analysis to assess human epidermal growth factor type 2 (HER2) gene expression. The accurate measurement of HER2 gene expression can assist physicians with treatment decisions for patients with cancers in tissues such as breast. For complete story, click here.
An article published in the Fall, 2008 issue of the Journal of Economic Perspectives concludes that improved behavior and increased screening among Americans are major contributors to the 13 percent decline in cancer mortality from 1990 to 2004 recently announced by the National Cancer Institute. In a study that is the first to evaluate the reasons for the decline, David Cutler of Harvard University examined data for breast, colorectal, lung and prostate cancer, and uncovered three factors leading to improved cancer survival. The most important of these is cancer screening, such as mammography and colonoscopy, which can detect cancer at an early, treatable stage. Second in importance is improved personal behavior, including a reduction in smoking. Dr Cutler ranks improved treatments, including surgery, chemotherapy and radiation as third in importance, and notes that their contribution comes at a high cost. "Drugs that are quite expensive have been shown to extend life by only a few months among patients with metastatic cancer, which raises questions about the relative value of such costly treatments," Dr Cutler stated. "In contrast, while screening can be expensive, increased screening has led to significantly longer life expectancy for those diagnosed early with colorectal or breast cancer."
"We typically think of the war on cancer as developing a new cure," Dr Cutler remarked. "An equally important question is figuring out how we can take what we know and make it work for more people. We should think about the war as not just developing the next weapon, but using what we have in a smarter way. A health care system working for cancer would prevent people from getting it, catch it early, and then treat people accordingly. If our healthcare system was focused in this way, there could be a huge benefit."
Minister for Health and Ageing, The Hon. Nicola Roxon MP, has announced that Australia would make a substantial contribution to the International Cancer Genome Consortium by tackling pancreatic cancer, one of the deadliest cancers and fourth most common cause of cancer death. The consortium brings together the world's leading scientists, through 11 funding organizations in 8 countries, and aims to catalogue the genetic changes of the 50 most common cancer types. The Australian team will be led by Professor Sean Grimmond from the University of Queensland's Institute for Molecular Bioscience in Brisbane and Professor Andrew Biankin from the Garvan Institute of Medical Research in Sydney. It will also involve collaborative contributions from the Walter and Eliza Hall Institute of Medical Research in Melbourne, Johns Hopkins University in Maryland, the Ontario Institute for Cancer Research and the University of California, San Francisco.
Professor Biankin, also a surgeon at Sydney's Bankstown Hospital, has treated hundreds of patients with pancreatic cancer. "It's a very aggressive cancer, killing around 90% of people within a year of diagnosis," he said. "Unlike the other common cancers, survival rates have not improved in over 30 years."
"Now that the technology and knowledge exists to process vast amounts of data quickly, it will allow us to uncover many of the triggers and genetic mechanisms underlying the disease, and therefore improve treatment."
The project is being funded through the National Health and Medical Research Council of Australia (NH&MRC), and at $27.5 million it is the largest single grant the NH&MRC has ever awarded. Further support will be provided by The Cancer Council NSW, the Queensland Government, the Garvan Institute and the University of Queensland. Applied Biosystems Inc. and Silicon Graphics, large international companies specialising in gene sequencing and array analysis and high performance computing systems respectively, are also making significant contributions.
Professor Rob Sutherland, Director of Garvan's Cancer Research Program, as well as Inaugural Director of the planned Garvan St. Vincent's Campus Cancer Centre, acknowledges the great potential for discovery. "We are thrilled to be part of an international team that is throwing its spotlight and resources on this particular cancer," he said.
"A decade ago, it took years to sequence one person's DNA, so we could only dream about identifying the detailed gene mutations that lead to the initiation and progression of different cancers. Today it's possible to sequence 500 hundred individual cases of 50 types of cancer in 5 years."
"While no-one is under the illusion that we'll cure all cancers within the next 5 years, this international collaboration will greatly accelerate progress."
"Some cancers may be cured, some will be targeted more effectively, others will be progressively demystified. Medical research is a long-term process of discovery."
The Garvan Institute of Medical Research was founded in 1963. Initially a research department of St Vincent's Hospital in Sydney, it is now one of Australia's largest medical research institutions with nearly 500 scientists, students and support staff. Garvan's main research programs are: Cancer, Diabetes & Obesity, Immunology and Inflammation, Osteoporosis and Bone Biology, and Neuroscience. The Garvan's mission is to make significant contributions to medical science that will change the directions of science and medicine and have major impacts on human health. The outcome of Garvan's discoveries is the development of better methods of diagnosis, treatment, and ultimately, prevention of disease.
Source: Alison Heather Research Australia
Research into the causes, prevention, and treatment of breast cancer is under way in many medical centers throughout the world. Causes of breast cancer
Studies continue to uncover lifestyle factors and habits that alter breast cancer risk. Ongoing studies are looking at the effect of exercise, weight gain or loss, and diet on breast cancer risk.
Studies on the best use of genetic testing for BRCA1 and BRCA2 mutations continue at a rapid pace. Other genes that contribute to breast cancer risk are also being identified. This will occur more rapidly now that the human genome has been sequenced.
Potential causes of breast cancer in the environment have also received more attention in recent years. While much of the science on this topic is still in its earliest stages, this is an area of active research.
A large, long-term study funded by the National Institute of Environmental Health Sciences (NIEHS) is now being done to help find the causes of breast cancer. Known as the Sister Study, it has enrolled 50,000 women who have sisters with breast cancer. This study will follow these women for at least 10 years and collect information about genes, lifestyle, and environmental factors that may cause breast cancer. An offshoot of the Sister Study, the Two Sister Study, is designed to look at possible causes of early onset breast cancer. To find out more about these studies, call 1-877-4-SISTER (1-877-474-7837) or visit the Sister Study Web site (www.sisterstudy.org).
Results of several studies suggest that selective estrogen-receptor modulators (SERMs) such as tamoxifen and raloxifene may lower breast cancer risk in women with certain breast cancer risk factors. But so far, many women are reluctant to take these medicines because they are concerned about possible side effects.
Newer studies are looking at whether aromatase inhibitors -- drugs such as anastrozole, letrozole, and exemestane -- can reduce the risk of developing breast cancer in post-menopausal women. These drugs are already being used as adjuvant hormone therapy to help prevent breast cancer recurrences, but none of them is approved for reducing breast cancer risk at this time.
Evirolimus (Afinitor®) is a new type of targeted therapy drug that was recently approved to treat kidney cancer. In one study, letrozole plus evirolimus worked better than letrozole alone in shrinking breast tumors before surgery. More studies using this drug are planned.
Fenretinide, a retinoid, is also being studied as a way to reduce the risk of breast cancer (retinoids are drugs related to vitamin A). In a small study, this drug reduced breast cancer risk as much as tamoxifen. Other drugs are also being studied to reduce the risk of breast cancer.
For more information, see the American Cancer Society document, Medicines to Reduce Breast Cancer Risk.
For women on HRT, tenderness may be warning sign By Julie Steenhuysen Tue Oct 13, 10:28 am ET
CHICAGO (Reuters) – Women whose breasts became tender after taking hormone replacement therapy had nearly twice the risk of developing breast cancer than women whose breasts did not become tender on the drugs, U.S. researchers said on Monday.
They said breast tenderness may be a way to identify women who have a higher risk of developing breast cancer while taking hormone replacement therapy to treat menopause.
"We report that an increase in breast tenderness, easily detected by physicians or patients, identifies a population at particular risk for breast cancer," Dr. Carolyn Crandall of the University of California Los Angeles and colleagues reported in the Archives of Internal Medicine.
The team analyzed data on the more than 16,000 women who took estrogen-plus-progestin as part of the widely publicized Women's Health Initiative or WHI study, which was halted in 2002 when researchers found healthy menopausal women who took the drugs were more likely to develop breast cancer.
Most of the women in the WHI studies took Premarin or Prempro made by Wyeth.
Doctors now recommend hormone replacement therapy for women suffering severe menopause symptoms, but caution that they should use the lowest dose possible for the shortest period of time.
Crandall and colleagues culled through the data to see if breast tenderness played a role in breast cancer risk. In the study, 8,506 took estrogen plus progestin and 8,102 got placebo pills.
The women had mammograms and breast exams at the start of the trial and every year after that. They reported whether they had breast tenderness at the beginning of the trial and a year later.
Based on their analysis, the researchers found women who took hormone treatments had triple the risk of developing breast tenderness.
And those who had breast tenderness after taking the pills were at 48 percent higher risk of invasive breast cancer than other women who took hormone replacement therapy.
The team said the relationship between breast tenderness and breast cancer risk was not clear.
It may be that hormone therapy is causing breast-tissue cells to multiply more rapidly, but the team could not tell that by the study, Crandall said.
"We need to figure out what makes certain women more susceptible to developing breast tenderness during hormone therapy," Crandall said in a statement.
The team said breast tenderness while taking combination hormone therapy "may be a marker of increased breast cancer risk," and women who develop breast tenderness after taking the drugs should consult their doctors about whether they should continue on the therapy.
Wyeth said in a statement that while the findings are interesting and may warrant further study, breast tenderness is not an established risk factor for breast cancer.
They said breast tenderness can occur in up to 25 percent of women after starting combined hormone therapy and is usually transient.
"Wyeth continues to support the appropriate use of hormone therapy and recommends that it be used at the lowest dose for the appropriate duration consistent with treatment goals and risks for the individual woman," the company said.
More than 400,000 women die from breast cancer globally each year. About 75 percent of breast cancers are estrogen-receptor positive, meaning they are fed by estrogen.
New bill to aid vets hurt by Agent Orange - by land & sea
BY Jake Pearson DAILY NEWS WRITER
Wednesday, October 28th 2009, 4:00 AM
Bobby Condon was a young kid from Flatbush when he enlisted in the U.S. Navy to fight in the Vietnam War.Nicknamed "Brooklyn" by fellow soldiers, Condon, now 63, has developed an Agent Orange-linked cancer - but was denied coverage by the Veterans Administration because he never set foot in Vietnam.
"I would have flown to Saigon and put my feet on the ground for 30 minutes [had I known]," said Condon, a flight operator on the USS Intrepid who last year was diagnosed with chronic lymphocytic leukemia (CLL), an incurable form of cancer. "But I was denied and I didn't get nothing."
This week, Sen. Kirsten Gillibrand will introduce legislation that will require coverage for the estimated 800,000 nationwide "blue-water vets," like Condon, who have illnesses linked to Agent Orange exposure but never set foot in Vietnam.
"Because of technicality in the law, hundreds of thousands of American veterans are being denied the health care benefits they need and deserve," said Gillibrand, adding there are about 13,500 such veterans in New York State.
The U.S. military dumped nearly 20 million gallons of the deadly herbicide to remove foliage during the Vietnam War. In 1991, Congress passed legislation requiring the VA to cover all sicknesses linked to Agent Orange exposure. But in 2002, the VA changed its policy to cover only those veterans who had "boots on the ground," excluding sailors and pilots such as Condon.
"I didn't even hear about Agent Orange until I came back," said Condon, who believes he got sick from working on planes that were flown through Agent Orange drop zones.
A spokesman for the VA wouldn't comment on pending legislation.