| Literature DB >> 23783119 |
Philippe Juin1, Olivier Geneste, Fabien Gautier, Stéphane Depil, Mario Campone.
Abstract
Cancer cells are subject to many apoptotic stimuli that would kill them were it not for compensatory prosurvival alterations. BCL-2-like (BCL-2L) proteins contribute to such aberrant behaviour by engaging a network of interactions that is potent at promoting survival but that is also fragile: inhibition of a restricted number of interactions may suffice to trigger cancer cell death. Currently available and novel compounds that inhibit these interactions could be efficient therapeutic agents if this phenotype of BCL-2L dependence was better understood at a molecular, cellular and systems level and if it could be diagnosed by relevant biomarkers.Entities:
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Year: 2013 PMID: 23783119 DOI: 10.1038/nrc3538
Source DB: PubMed Journal: Nat Rev Cancer ISSN: 1474-175X Impact factor: 60.716