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dc.contributor.authorMerino, Delphine-
dc.contributor.authorKelly, Gemma L-
dc.contributor.authorLessene, Guillaume-
dc.contributor.authorWei, Andrew H-
dc.contributor.authorRoberts, Andrew W-
dc.contributor.authorStrasser, Andreas-
dc.identifier.citationCancer cell 2018; 34(6): 879-891-
dc.description.abstractDefects 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.-
dc.subjectBH3-mimetic drugs-
dc.subjectBH3-only proteins-
dc.titleBH3-Mimetic Drugs: Blazing the Trail for New Cancer Medicines.-
dc.typeJournal Article-
dc.identifier.journaltitleCancer cell-
dc.identifier.affiliationDepartment of Medical Biology, The University of Melbourne, Parkville, VIC 3010, Australiaen
dc.identifier.affiliationClinical Haematology, Peter MacCallum Cancer Centre and Royal Melbourne Hospital, Melbourne, VIC 3000, Australiaen
dc.identifier.affiliationVictorian Comprehensive Cancer Centre, Melbourne, VIC 3000, Australiaen
dc.identifier.affiliationDepartment of Haematology, Alfred Hospital and Monash University Melbourne, Melbourne, VIC 3004, Australiaen
dc.identifier.affiliationThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australiaen
dc.identifier.affiliationOlivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationSchool of Cancer Medicine, La Trobe University, Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Medical Biology, The University of Melbourne, Parkville, VIC 3010, Australiaen
dc.identifier.affiliationDepartment of Pharmacology and Therapeutics, The University of Melbourne, Parkville, VIC 3010, Australiaen
dc.type.austinJournal Article-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
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