Abstract

There have long been indications of a role for PI3K (phosphatidylinositol 3-kinase) in cancer pathogenesis. Experimental data document a requirement for deregulation of both transcription and translation in PI3K-mediated oncogenic transformation. The recent discoveries of cancer-specific mutations in PIK3CA, the gene that encodes the catalytic subunit p110 of PI3K, have heightened the interest in the oncogenic potential of this lipid kinase and have made p110 an ideal drug target.

Author affiliations

1. Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA.

Correspondence to: Peter K. Vogt¹ Email: pkvogt@scripps.edu

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