Journal
CANCER CELL
Volume 34, Issue 6, Pages 879-891Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2018.11.004
Keywords
-
Categories
Funding
- National Health and Medical Research Council (NHMRC), Australia [NHMRC 1101378]
- NHMRC [1086291, 1116937, 1113133, 1143105, 1126843, 1117089]
- Cancer Council Victoria [1086157, 1147328, 1102104]
- Leukemia Foundation Australia
- VCA [MCRF 17028]
- Leukemia & Lymphoma Society Special Center of Research [7015-18]
- Medical Research Future Fund [1141460]
- VCA
- Australian Cancer Research Foundation
- National Health and Medical Research Council of Australia [1143105, 1126843, 1117089, 1116937, 1086291] Funding Source: NHMRC
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available
Share Paper
