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Title: BH3-Mimetic Drugs: Blazing the Trail for New Cancer Medicines.
Austin Authors: Merino, Delphine;Kelly, Gemma L;Lessene, Guillaume;Wei, Andrew H;Roberts, Andrew W;Strasser, Andreas
Affiliation: Department of Medical Biology, The University of Melbourne, Parkville, VIC 3010, Australia
Clinical Haematology, Peter MacCallum Cancer Centre and Royal Melbourne Hospital, Melbourne, VIC 3000, Australia
Victorian Comprehensive Cancer Centre, Melbourne, VIC 3000, Australia
Department of Haematology, Alfred Hospital and Monash University Melbourne, Melbourne, VIC 3004, Australia
The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australia
Olivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australia
School of Cancer Medicine, La Trobe University, Melbourne, Victoria, Australia
Department of Medical Biology, The University of Melbourne, Parkville, VIC 3010, Australia
Department of Pharmacology and Therapeutics, The University of Melbourne, Parkville, VIC 3010, Australia
Issue Date: 10-Dec-2018
Publication information: Cancer cell 2018; 34(6): 879-891
Abstract: Defects in apoptotic cell death can promote cancer and impair responses of malignant cells to anti-cancer therapy. Pro-survival BCL-2 proteins prevent apoptosis by keeping the cell death effectors, BAX and BAK, in check. The BH3-only proteins initiate apoptosis by neutralizing the pro-survival BCL-2 proteins. Structural analysis and medicinal chemistry led to the development of small-molecule drugs that mimic the function of the BH3-only proteins to kill cancer cells. The BCL-2 inhibitor venetoclax has been approved for treatment of refractory chronic lymphocytic leukemia and this drug and inhibitors of pro-survival MCL-1 and BCL-XL are being tested in diverse malignancies.
DOI: 10.1016/j.ccell.2018.11.004
Journal: Cancer cell
PubMed URL: 30537511
Type: Journal Article
Subjects: BCL-2
BH3-mimetic drugs
BH3-only proteins
Appears in Collections:Journal articles

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