Research ArticleCancer

PIK3CA mutations enable targeting of a breast tumor dependency through mTOR-mediated MCL-1 translation

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Science Translational Medicine  14 Dec 2016:
Vol. 8, Issue 369, pp. 369ra175
DOI: 10.1126/scitranslmed.aae0348

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Sneak attack on breast cancer’s defense

The usual goal of cancer treatment is to kill malignant cells, not just slow down their growth. A class of drugs called BH3 mimetics serves this purpose by inhibiting antiapoptotic proteins and thus helping drive the cells toward apoptosis (programmed cell death). MCL-1 is an antiapoptotic protein that is not targeted by currently bioavailable BH3 mimetics, and it is often responsible for resistance to these drugs. Anderson et al. have discovered that breast cancers with the commonly observed PIK3CA mutations can be treated with mTOR inhibitors to suppress MCL-1, leaving the cells vulnerable to BH3 mimetics and subsequent induction of apoptosis, both directly and in combination with chemotherapy.

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