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Bcl-XL represents a druggable molecular vulnerability during aurora B inhibitor-mediated polyploidization

28 Jun 2010

Abstract excerpt

Aurora kinase B inhibitors induce apoptosis secondary to polyploidization and have entered clinical trials as an emerging class of neocytotoxic chemotherapeutics. We demonstrate here that polyploidization neutralizes Mcl-1 function, rendering cancer cells exquisitely dependent on Bcl-XL/-2. This "addiction" can be exploited therapeutically by combining aurora kinase inhibitors and the orally bioavailable BH3...

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PMID: 20616035
DOI: 10.1073/pnas.0913615107

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