PI3K in cancer: divergent roles of isoforms, modes of activation and therapeutic targeting

Nat Rev Cancer. 2015 Jan;15(1):7-24. doi: 10.1038/nrc3860.

Lauren M Thorpe ¹, Haluk Yuzugullu ², Jean J Zhao ²

Affiliations

1 1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA. [2] Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA. [3] Program in Virology, Harvard Medical School, Boston, Massachusetts 02115, USA.
2 1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA. [2] Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA.

PMID: 25533673 DOI: 10.1038/nrc3860

Abstract

Phosphatidylinositol 3-kinases (PI3Ks) are crucial coordinators of intracellular signalling in response to extracellular stimuli. Hyperactivation of PI3K signalling cascades is one of the most common events in human cancers. In this Review, we discuss recent advances in our knowledge of the roles of specific PI3K isoforms in normal and oncogenic signalling, the different ways in which PI3K can be upregulated, and the current state and future potential of targeting this pathway in the clinic.

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