Journal
CANCER RESEARCH
Volume 67, Issue 7, Pages 2908-2911Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-07-0082
Keywords
-
Categories
Funding
- NATIONAL CANCER INSTITUTE [R01CA100866, R01CA063753, R01CA093738] Funding Source: NIH RePORTER
- NCI NIH HHS [CA 100866, CA 93738, CA63753] Funding Source: Medline
Ask authors/readers for more resources
ABT-737 targets Bcl-2/Bcl-xL but not Mcl-1, which confers resistance to this novel agent. Here, we summarize recent findings indicating that Mcl-1 represents a critical determinant of ABT-737 sensitivity and resistance, and that Mcl-1 down-regulation by various pharmacologic agents or genetic approaches dramatically increases ABT-737 lethality in diverse malignant cell types. These findings also show that the multidomain proapoptotic proteins Bax and Bak play important functional roles in ABT-737-mediated apoptosis, and that Bak activation is essential in potentiation of ABT-737 lethality by agents that down-regulate Mcl-1. Collectively, these findings suggest a novel therapeutic strategy targeting multiple arms of the apoptotic machinery.
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