Mutation of the PIK3CA oncogene in human cancers - PubMed (original) (raw)

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Mutation of the PIK3CA oncogene in human cancers

B Karakas et al. Br J Cancer. 2006.

Abstract

It is now well established that cancer is a genetic disease and that somatic mutations of oncogenes and tumour suppressor genes are the initiators of the carcinogenic process. The phosphatidylinositol 3-kinase signalling pathway has previously been implicated in tumorigenesis, and evidence over the past year suggests a pivotal role for the phosphatidylinositol 3-kinase catalytic subunit, PIK3CA, in human cancers. In this review, we analyse recent reports describing PIK3CA mutations in a variety of human malignancies, and discuss their possible implications for diagnosis and therapy.

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Figure 1

Figure 1

(A) The main reaction catalysed by PI3K: phosphatidylinositol (PI) 4,5 bisphosphate (PIP2) to phosphatidylinositol (PI) 3,4,5-triphosphate (PIP3). (B) PI3K is activated upon ligand binding to a receptor tyrosine kinase (RTK), which then activates the regulatory subunit (p85) to bind the catalytic p110_α_ subunit. This ultimately triggers various downstream signalling cascades resulting in cell survival, apoptosis, transformation, metastasis, and cell migration. (C) Schematic representation of PIK3CA (p110_α_ catalytic subunit of PI3K) and its functional domains with the most common somatic mutations, E542K, E545K and H1047R within the helical and kinase domains indicated.

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