November 11 - 14, 2008
Hyatt Regency Cambridge
Lewis C. Cantley, Harvard Medical School, Boston, MA
Charles L. Sawyers, Memorial Sloan-Kettering Cancer Center, New York, NY
Mutations in genes that encode components of the phosphoinositide 3-kinase (PI3K) pathway are perhaps the most frequent events observed in solid tumors. The PI3K pathway can be activated by overproduction of growth factors or chemokines or by mutations in growth factor receptors, Ras, PTEN, or PI3K itself. Activation of this pathway contributes to cell growth, cell cycle entry, cell survival, and cell motility, all important aspects of tumorigenesis. However, progress is being made as several small molecule inhibitors of Class Ia PI3K enzymes have recently entered phase I clinical trials.
This AACR Special Conference assembled prominent investigators to discuss recent advances in this rapidly growing area. Sessions focused on the basic research studying the role of PI3K and related pathways in cancer. Discussions also explored strategies for determining which patients are most likely to respond to PI3K inhibitors. In addition, the advantages and disadvantages of targeting specific PI3K enzymes, versus other families of enzymes, was discussed. This conference provided a unique forum to review the remarkable progress in this area over the past few years, and provided a glimpse of where the field is moving.
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Please visit the AACR Meetings & Workshops Calendar for a complete list of upcoming programs.