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... [read more]

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 will assemble prominent investigators to discuss recent advances in this rapidly growing area. Sessions will focus on the basic research which is studying the role of PI3K/mTOR and related pathways in cancer. Discussions will also explore strategies for determining which patients are most likely to respond to PI3K pathway inhibitors. A special session has been set aside for late-breaking presentations and there will be ample time for discussion. This conference will provide a unique forum to review the remarkable progress in this area over the past few years, and provide a glimpse of where the field is moving.