Journal article
Targeting BCL-2-like Proteins to Kill Cancer Cells
S Cory, AW Roberts, PM Colman, JM Adams
Trends in Cancer | CELL PRESS | Published : 2016
Abstract
Mutations that impair apoptosis contribute to cancer development and reduce the effectiveness of conventional anti-cancer therapies. These insights and understanding of how the B cell lymphoma (BCL)-2 protein family governs apoptosis have galvanized the search for a new class of cancer drugs that target its pro-survival members by mimicking their natural antagonists, the BCL-2 homology (BH)3-only proteins. Successful initial clinical trials of the BH3 mimetic venetoclax/ABT-199, specific for BCL-2, have led to its recent licensing for refractory chronic lymphocytic leukemia and to multiple ongoing trials for other malignancies. Moreover, preclinical studies herald the potential of emerging B..
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Funding Acknowledgements
We warmly thank our WEHI colleagues for their many contributions to the research and ideas underpinning this review and apologize to any colleagues whose findings could not be cited owing to space constraints. Work in the authors' laboratories was supported by fellowship and grants from the National Health and Medical Research Council (461221, 1016701, 1016647, 1079560, 1041797), the Leukemia & Lymphoma Society (SCOR 7001-13), the Victorian Cancer Agency, the Cancer Council Victoria and the Australian Cancer Research Foundation. Research infrastructure at WEHI is supported by annual grants from the governments of Australia (IRIISS grant 9000220) and Victoria (OIS grant).