“AMA, March of Dimes and Others Support ACLU Challenge to Patents on ... - Common Dreams” plus 4 more |
- AMA, March of Dimes and Others Support ACLU Challenge to Patents on ... - Common Dreams
- Revolutionary Breast Cancer Drug Within 2 Years - Med India
- Chemotherapy resistance: Checkpoint protein provides armor against ... - PhysOrg
- Small Peptide Found To Stop Lung Cancer Tumor Growth In Mice - Science Daily
- Side Effect Seen in Breast Cancer Drug - AOL
| AMA, March of Dimes and Others Support ACLU Challenge to Patents on ... - Common Dreams Posted: 27 Aug 2009 08:42 AM PDT NEW YORK - August 27 - The American Civil Liberties Union and the Public Patent Foundation (PUBPAT), a not-for-profit organization affiliated with Benjamin N. Cardozo School of Law, filed a motion asking a federal court to rule that patents on two human genes associated with breast and ovarian cancer are unconstitutional and invalid. Several major organizations, including the American Medical Association (AMA), the March of Dimes and the American Society for Human Genetics (ASHG), are filing friend-of-the-court briefs in support of the motion for summary judgment. The groups charge that the patents stifle diagnostic testing and research that could lead to cures and that they limit women's options regarding their medical care. "When you patent genes, you are really patenting knowledge," said Chris Hansen, an attorney with the ACLU. "Granting patents on human genes limits scientific research, learning and the free flow of information. We hope the court rules soon that patents are meant to protect inventions, not things that exist in nature like genes in the human body." The lawsuit, Association for Molecular Pathology, et al. v. U.S. Patent and Trademark Office, et al., was originally filed on May 12 in the U.S. District Court for the Southern District of New York on behalf of breast cancer and women's health groups, individual women and scientific associations representing approximately 150,000 researchers, pathologists and laboratory professionals. The lawsuit was filed against the U.S. Patent and Trademark Office, as well as Myriad Genetics and the University of Utah Research Foundation, which hold the patents on the BRCA genes. The lawsuit charges that patents on human genes violate the First Amendment and patent law because genes are "products of nature." "Human genes are products of nature and patents on them should never have been granted in the first place," said Daniel B. Ravicher, Executive Director of PUBPAT and co-counsel in the lawsuit. "There is something fundamentally wrong with companies being able to own the rights to a piece of the human genome. Genes are not inventions, and patenting genetic sequences is like patenting blood, air or water." Mutations along the genes, known as BRCA1 and BRCA2, are responsible for most cases of hereditary breast and ovarian cancers. Many women with a history of breast and ovarian cancer in their families opt to undergo genetic testing to determine if they have the mutations on their BRCA genes that put them at increased risk for these diseases. This information is critical in helping these women decide on a plan of treatment or prevention, including increased surveillance or preventive mastectomies or ovary removal. The patents granted to Myriad give the company the exclusive right to perform diagnostic tests on the BRCA1 and BRCA2 genes and to prevent any researcher from even looking at the genes without first getting permission from Myriad. Myriad's monopoly on the BRCA genes makes it impossible for women to access alternate tests or get a second opinion about their results and allows Myriad to charge a high rate for their tests. "The AMA is concerned that medical patents on genes could harm patients' access to care," said Rebecca Patchin, M.D, AMA Board Chair. "Physicians should not be stifled in what care they can provide because someone has patented a part of human biology. These patents are too broad and should be reined in so that no patient is denied care." Dr. Edward McCabe of UCLA, President of ASHG, said, "The American Society of Human Genetics includes thousands of members who do basic research as well as those who are involved in clinical and patient care. The deterrents presented by the patenting and exclusive licensing of BRCA genes continue to cause problems in many laboratories. ASHG is therefore a party to the amicus brief with other large and representative medical and research organizations." Because the ACLU's lawsuit challenges the whole notion of gene patenting, its outcome could have far reaching effects beyond the patents on the BRCA genes. Approximately 20 percent of all human genes are patented, including genes associated with Alzheimer's disease, muscular dystrophy, colon cancer, asthma and many other illnesses. Nobel Prize winner Sir John Sulston, Chair of the Institute for Science, Ethics and Innovation at the University of Manchester, who supports the ACLU's lawsuit, said, "Patents on human genes are harmful to the practice of science and a disincentive to further research on those genes. Patents on genes inhibit access to the most basic information and discourage scientific communication and data sharing. Free sharing of this information is vital to understanding the role of genetic variations in human disease." Attorneys on the case include Hansen and Aden Fine of the ACLU First Amendment Working Group; Lenora Lapidus and Sandra Park of the ACLU Women's Rights Project; and Ravicher of PUBPAT. Tania Simoncelli, the ACLU's science advisor, provides expert guidance on the case. More information about the case, including an ACLU video featuring breast cancer patients, plaintiff and supporter statements and declarations, the motion for summary judgment and the legal complaint, can be found online at: www.aclu.org/brca  This posting includes an audio/video/photo media file: Download Now |
| Revolutionary Breast Cancer Drug Within 2 Years - Med India Posted: 27 Aug 2009 07:23 AM PDT [fivefilters.org: unable to retrieve full-text content] A major breakthrough in search of a cure for breast cancer has been made by Brit scientists, who may develop a drug within two years to beat the life threatening disease. Instead of looking at how to stop tumours from forming, the new study has found ... This posting includes an audio/video/photo media file: Download Now |
| Chemotherapy resistance: Checkpoint protein provides armor against ... - PhysOrg Posted: 27 Aug 2009 10:01 AM PDT Chemotherapy resistance: Checkpoint protein provides armor against cancer drugsAugust 27th, 2009 These tumors with low levels of Fbx6 are unable to degrade the checkpoint protein Chk1 making them resistant to certain cancer drugs. Credit: Image: Courtesy of Dr. Youwei Zhang, Case Western Reserve University. Cell cycle checkpoints act like molecular tripwires for damaged cells, forcing them to pause and take stock. Leave the tripwire in place for too long, though, and cancer cells will press on regardless, making them resistant to the lethal effects of certain types of chemotherapy, according to researchers at the Salk Institute for Biological Studies. Their findings, published in the Aug. 28 issue of Molecular Cell, help explain how the checkpoint exit is delayed in some cancer cells, helping them to recover and resume dividing after treatment with DNA-damaging cancer drugs. "A lot of progress has been made in understanding the molecular details of checkpoint activation," says senior author Tony Hunter, Ph.D., a professor in the Molecular and Cell Biology Laboratory, "but checkpoint termination, which is essential for the resumption of cell cycle progression, is less well understood." The Salk researchers say that a better understanding of this crucial process may allow them to develop biological markers that predict clinical resistance to chemotherapy and to design cancer drugs with fewer side effects by exploiting the molecular mechanism underlying the checkpoint exit. "If we could screen tumors for markers of chemo-resistance, we could then adjust the treatment accordingly," hopes first author You-Wei Zhang, Ph.D., formerly a postdoctoral researcher in Hunter's lab and now an assistant professor at Case Western Reserve University in Cleveland, Ohio. In response to DNA damage and blocked replicationthe process that copies DNAeukaryotes activate the DNA damage checkpoint pathway, which stops the cell cycle, buying time to repair damage and recover from stalled or collapsed replication forks. If not repaired, these errors can either kill a cell when it attempts to divide or lead to genomic instability and eventually cancer. A key role in this process is played by the checkpoint protein Chk1, which responds to stressful conditions induced by hypoxia, DNA damage-inducing cancer drugs, and irradiation. These same conditions set the protein up for eventual degradation. But how the cellular protein degradation machinery knows that it is time to dispose of activated Chk1 was unclear. In his experiments, Zhang discovered that activation of Chk1 exposes a so-called degron, a specific string of amino acids that attracts the attention of a protein known as Fbx6, short for F box protein 6. Fbx6 in turn brings in an enzyme complex that flags Chk1 proteins for degradation, allowing the cell to get rid of the activated checkpoint protein. Once Chk1 is eliminated, cells will resume the cell cycle progression, or, in the prolonged presence of replication stress, undergo programmed cell death. Yet some cancer cells keep dividing even in the presence of irreparable damage.
"Camptothecins are FDA-approved cancer drugs that induce replication stress and stop cancer cells dividing, but their clinical antitumor activity is very limited by the relatively rapid emergence of drug resistance, and the mechanisms are poorly understood," says Hunter. "We wondered whether defects in the Chk1 destruction machinery might allow cells to ignore the effects of camptothecin and similar drugs used for chemotherapy." When Zhang checked cultured cancer cell lines and breast cancer tissue, he found that low levels of Fbx6 predicted high levels of Chk1 and vice versa. But most importantly, he was able to demonstrate that two of the three most camptothecin-resistant cancer cell lines in the cancer cell line panel available through the National Cancer Institute displayed significant defects in camptothecin-induced Chk1 degradation, which seemed to be caused by very low levels of Fbx6 expression. "Chk1 and Fbx6 clearly play an important role for the regulation of the response to chemotherapy," he says. "One day, they could become an important prognostic marker that predicts patients' responsiveness to drugs such as irinotecan, platinum compounds, and gemcitabine, while Chk1 inhibitors might increase tumor cells' sensitivity to these drugs." Such a combination therapy could overcome clinical resistance or allow doctors to reduce the amount of administered drug, thereby reducing the often debilitating side effects. Source: Salk Institute (news : web)  This posting includes an audio/video/photo media file: Download Now |
| Small Peptide Found To Stop Lung Cancer Tumor Growth In Mice - Science Daily Posted: 27 Aug 2009 07:59 AM PDT ScienceDaily (Aug. 27, 2009) — In new animal research done by investigators at Wake Forest University School of Medicine, scientists have discovered a treatment effective in mice at blocking the growth and shrinking the size of lung cancer tumors, one of the leading causes of cancer death in the world. The study, recently published in Molecular Cancer Therapeutics, a journal of the American Association for Cancer Research, is the first to show that treatment with a specific peptide, angiotensin-(1-7), reduces lung tumor growth by inhibiting blood vessel formation. "If you're diagnosed with lung cancer today, you've got a 15 percent chance of surviving five years – and that's just devastating," said co-lead investigator Patricia E. Gallagher, Ph.D., director of the Molecular Biology Core Laboratory in the Hypertension and Vascular Research Center at the School of Medicine. "Those other 85 people – 85 percent – they're not going to see their kids graduate. They're not going to see their children get married." The lung cancer survival rate has changed little in the past 30 years, said Gallagher's co-lead investigator, E. Ann Tallant, Ph.D., a professor in the Hypertension and Vascular Research Center – a fact that motivates them in their research. Peptides, found in all animals, are compounds formed by linking one or more amino acids together through the sharing of electrons. They are among the building blocks of life. Peptides can perform a wide range of functions in the body, depending on which amino acids are involved. Some can regulate hormones, for example, while others can have an antibiotic function. Angiotensin-(1-7) is a small peptide that binds to proteins on the surface of cells and prevents cell growth – but only if the cell is actively growing when the binding occurs. That property is what led Tallant and Gallagher to explore the peptide's uses for treating cancer by blocking tumor growth. Angiotensin-(1-7) works by inhibiting the production of signals sent out by a cancer tumor for food. For tumors to grow, they need nutrients delivered by blood vessels. The signals they send prompt blood vessels to grow and invade the tumor to feed it. Every day during the six-week study, researchers injected either saline or the angiotensin (1-7) peptide into mice growing human lung cancer tumors. Over the course of the study, the tumors treated with angiotensin-(1-7) shrunk, while the saline-treated tumors grew and, at the end of the study, the tumors treated with angiotensin-(1-7) weighed about 60 percent less than the tumors treated with saline. Analysis also showed that the tumors from mice treated with the peptide had significantly fewer blood vessels compared to the tumors from the saline-treated animals. The researchers further tested angiotensin (1-7)'s affect on blood vessel formation, or angiogenesis, by treating chick embryos with the peptide – a procedure considered the gold standard for determining anti-angiogenic ability. They found that blood vessels continued to grow in a saline-injected control group, while blood vessel formation decreased by more than 50 percent in the embryos treated with angiotensin-(1-7). Tallant and Gallagher said the treatment likely has applications beyond lung cancer – they have collected data showing it is effective on breast, colon and brain tumors, as well. The treatment also presents an attractive possibility for future human cancer therapy from a cost perspective, they said. "Because it's a peptide, it's very small and can be made very easily," Gallagher said. "We sometimes like to say we're the aspirin of cancer therapy." Co-investigators on the study were graduate students David R. Soto-Pantoja and Jyotsana Menon of the School of Medicine. The study was funded by the Susan G. Komen Breast Cancer Research Foundation, Department of Defense, National Institutes of Health, Unifi, Farley-Hudson Foundation, and Golfers Against Cancer of the Triad. The first clinical trial of angiotensin-(1-7) has been completed at the School of Medicine and the results are currently being reviewed.  This posting includes an audio/video/photo media file: Download Now |
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