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SIGNAL TRANSDUCTION AND TARGETED THERAPY
Volume 2, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sigtrans.2017.63
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Class I phosphoinositide 3-kinase (PI3K) enzymes have attracted considerable attention as drug targets in cancer therapy over the last 20 years. The signaling pathway triggered by class I PI3Ks is dysregulated in a range of tumor types, impacting cell proliferation, survival and apoptosis. Frequent oncogenic mutations of PIK3CA have previously been discovered. In contrast, reports of PIK3CB mutations have been limited; however, in most cases, those that have been identified have been shown to be activating and oncogenic. The functional characterization of a PIK3CB catalytic domain mutant, p110 beta(E1051K), first discovered by others in castrate-resistant prostate cancer (mCRPC), is outlined in this report; our data suggest that p110 beta(E1051K) is a gain-of-function mutation, driving PI3K signaling, tumorigenic cell growth and migration. Tumor cells expressing p110 beta(E1051K) are sensitive to p110 beta inhibition; its characterization as an oncogenic driver adds to the rationale for targeting p110 beta and indicates a continuing need to further develop specific PI3K inhibitors for clinical development in cancer therapy.
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