Journal
CLINICAL CANCER RESEARCH
Volume 20, Issue 18, Pages 4740-4746Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1078-0432.CCR-13-1727
Keywords
-
Categories
Funding
- NIH [CA042978, CA179193, CA175747, CA142928, CA148805]
- Lustgarten Pancreatic Cancer Foundation
- Pancreatic Cancer Action Network-AACR
- Tempur-Pedic Retailers [12-60-25-DER]
- Ruth L. Kirschstein National Research Service Award [1F31CA180628]
Ask authors/readers for more resources
Cancers driven by oncogenic Ras proteins encompass some of the most deadly human cancer types, and there is a pressing need to develop therapies for these diseases. Although recent studies suggest that mutant Ras proteins may yet be druggable, the most promising and advanced efforts involve inhibitors of Ras effector signaling. Most efforts to target Ras signaling have been aimed at the ERK mitogen-activated protein kinase and the phosphoinositide 3-kinase signaling networks. However, to date, no inhibitors of these Ras effector pathways have been effective against RAS-mutant cancers. This ineffectiveness is due, in part, to the involvement of additional effectors in Ras-dependent cancer growth, such as the Rac small GTPase and the p21-activated serine-threonine kinases (PAK). PAK proteins are involved in many survival, cell motility, and proliferative pathways in the cell and may present a viable new target in Ras-driven cancers. In this review, we address the role and therapeutic potential of Rac and group I PAK proteins in driving mutant Ras cancers. (C)2014 AACR.
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