The American Association for Cancer Research (AACR) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education activities for physicians.
Credit Designation Statement
AACR has designated this live activity for a maximum of 17.0 AMA PRA Category 1 Credit(s)™. Physicians should only claim credit commensurate with the extent of their participation in the activity.
Credit certification for individual sessions may vary, dependent upon compliance with the ACCME Accreditation Criteria. The final number of credits may vary from the maximum number indicated above.
Claiming (CME) Credit
Physicians and other health care professionals seeking AMA PRA Category 1 Credit(s)TM for this live continuing medical education activity must complete the CME Request for Credit Survey by Friday, January 11, 2019. Certificates will only be issued to those who complete the survey. The Request for Credit Survey will be available via a link on this website and via email. Your CME certificate will be sent to you via email after the completion of the activity.
Statement of Educational Need, Target Audience, and Learning Objectives
Genetic events leading to aberrant activation of the phosphoinositide 3-kinase (PI3K)/mTOR signaling pathway are among the most frequently occurring alterations in human cancers. In normal cells, this pathway responds to growth factors, cytokines, and hormones, such as insulin, and promotes cell growth, proliferation, survival, and metabolism through a variety of downstream targets. Oncogenic mutations in cancer cells activate this pathway in a manner that disconnects its control of these cellular processes from normal growth signals, leading to constitutive activation of the pathway. Cancer genome sequencing efforts combined with numerous preclinical and clinical studies have highlighted the importance of this pathway in cancer development and progression.
From molecular and cell biologic studies, it has become increasingly clear that PI3K is not part of a linear pathway but rather a key component of a broader network of signaling pathways, with intimate connections to the mechanistic target of rapamycin (mTOR) and Ras pathways, among others. PI3K and mTOR are particularly intertwined, with the mTOR protein complexes (mTORC1 and mTORC2), acting as both downstream effectors and central regulators of the pathway. Furthermore, while PI3K is predominantly a lipid kinase and mTOR is a protein kinase, these two proteins are structurally related to each other, such that chemical inhibitors can often directly inhibit the activity of both proteins. mTOR signaling is elevated in the majority of human cancers, and this occurs, in part, through oncogenic activation of the PI3K pathway. The focus of this meeting is on understanding and targeting the PI3K-mTOR network in cancer.