American Association for Cancer Research

Targeting PI3K/mTOR Signaling in Cancer

Targeting PI3K/mTOR Signaling in Cancer 2011

February 24-27, 2011
Hyatt Regency San Francisco
San Francisco, CA

CO-CHAIRPERSONS:
Lewis C. Cantley, Beth Israel Deaconess Medical Center, Boston, MA
Funda Meric-Bernstam, University of Texas MD Anderson Cancer Center, Houston, TX
David M. Sabatini, Whitehead Institute for Biomedical Research, Cambridge, MA

Alterations in phosphoinositide 3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling are perhaps the most frequent events observed in solid tumors. The PI3K/mTOR pathway can be activated by overproduction of growth factors or chemokines, loss of INPP4B or PTEN expression, 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. Rapamycin analogs have already been shown to have antitumor efficacy in some tumor types. New generation PI3K, Akt, and mTOR inhibitors have shown significant promise preclinically and are now in clinical trials.

This AACR Special Conference assembled over 450 investigators from around the world to discuss recent advances in this rapidly growing area. Sessions focused on the basic research studying the role of PI3K/mTOR and related pathways in cancer. Discussions explored strategies for determining which patients are most likely to respond to PI3K pathway inhibitors. The 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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