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Archive - Apr 28, 2012

San Francisco Personalized Medicine Conference 5.0 Will Focus on Epigenetics

The fifth annual Personalized Medicine Conference (5.0) hosted by San Francisco State University, this year with a focus on epigenetics, will be held on Thursday, May 24, 2012 from 8:00 am to 7:30 pm at the South San Francisco Conference Center. To view the conference website and to register for the conference, please go to http://personalizedmedicine.sfsu.edu/. Scheduled speakers include Michael Snyder, M.D., Ph.D., Chair/Director, Department of Genetics & Stanford Center for Genomics and Personalized Medicine, Stanford University; Brian Kennedy, Ph.D., CEO, Buck Institute for Age Research; Cristina Gentilini, Ph.D., Commercial Research Scientist, Swedish Biomimetics 3000; Jorge A. Leon, President/CEO, Leomics Associates, Inc.; and Stephen M. Anderson, Ph.D., CSO of Oncology and Genetics, LabCorp. The organizers note that epigenetics, or genetic changes above and beyond the DNA sequence level, have profound implications for personalized medicine, pharmacogenomics, aging, and oncology. While personalized medicine is poised to transform healthcare over the next several decades, it has become abundantly clear that the DNA sequence itself is only part of the story. The regulation of gene expression, and how it changes in health and disease, and in response to therapy, are crucial. The organizers invite you to attend this conference and learn the latest information on how epigenetics is and will be impacting personalized medicine. The conference will also be an excellent networking opportunity for health and industry professionals, educators, and scientists. Seating is limited and if you register early, you can save $100 on the registration fee. Sponsors of the conference include Genentech, Celgene, LabCorp, and BioMarin, among many others.

“Single Most Dramatic Improvement in the Treatment of Melanoma in 20 Years"

At Moffitt Cancer Center in Tampa, Florida, patients with stage III and IV unresectable melanoma are now routinely genetically profiled for several gene mutations, including ones in the BRAF gene, a known driver oncogene for melanoma. Research has shown that mutations in the BRAF gene determine sensitivity or resistance to a class of drugs that are BRAF inhibitors. "We have found that a large number of patients with melanoma who have the BRAF gene mutation quickly develop resistance to drugs that are BRAF inhibitors," said Jeffrey S. Weber, M.D., Ph.D., director of the Donald A. Adam Comprehensive Melanoma Research Center at Moffitt. "A recent approach in the melanoma research community is to find ways to overcome resistance to drugs we targeted to mutated BRAF." At Moffitt, researchers have access to a large database of patient-donated tissues through Moffitt's Total Cancer Care™ program, a far-reaching design for care that includes building a biorepository of tumor samples for study and patient selection for clinical trials participation. By looking for patient genetic profiles for BRAF, Moffitt researchers are working at the frontiers of personalized medicine, which is the effort to match the right patient to the right drug. According to Dr. Weber, although 50 percent of melanoma patients might have the BRAF mutation, the lack of other valid molecular targets for melanoma has "hampered efforts to individualize therapy." That may have changed now that the U.S. Food and Drug Administration has approved the drug Vemurafenib for melanoma patients who test positive for the BRAF mutation. An international team of researchers, including those at Moffitt led by Dr.