Prof. Lewis C. Cantley

Prof. Lewis C. Cantley

Professor of Cancer Biology in Medicine and is the Meyer Director of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine

Lewis Cantley has made significant advances in cancer research, stemming from his discovery of the signaling pathway phosphoinositide 3-kinase (PI3K) in 1984. His pioneering research has resulted in revolutionary treatments for cancer, diabetes and autoimmune diseases.

The author of over 400 original papers and more than 50 book chapters and review articles, Dr. Cantley is a fellow of the American Academy of Arts and Sciences and a member of the National Academy of Sciences. He graduated summa cum laude with a B.S. in chemistry from West Virginia Wesleyan College (1971) and obtained a Ph.D. in biophysical chemistry from Cornell University (1975).

He conducted postdoctoral research at Harvard University, where he was appointed assistant professor of biochemistry and molecular biology in 1978.

He became a professor of physiology at Tufts University in 1985, but returned to Harvard Medical School as professor of cell biology in 1992.

He became chief of Harvard’s new Division of Signal Transduction, and a founding member of its Department of Systems Biology in 2002.

In 2007, he was appointed director of the Beth Israel Deaconess Cancer Center. He joined the faculty of Weill Cornell Medical College and NewYork-Presbyterian Hospital in 2012

 

ABSTRACT

 

Title: PI 3-Kinase and Cancer Metabolism

Summary: Phosphoinositide 3-Kinase (PI3K) is activated by insulin and other growth factors to mediate cell growth. The PI3K enzyme encoded by the PIK3CA gene is one of the most frequently mutated oncogenes in human cancer.

This same enzyme mediates insulin responses in liver, muscle, fat and other tissues and drugs that inhibit this enzyme have the expected effect of raising serum glucose and insulin levels.

Data will be presented showing that dietary and pharmaceutical interventions that limit elevation of serum insulin improve responses to PI3K inhibitors in mouse models of cancer by preventing insulin-dependent activation of PI3K in tumors.

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