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Trends Cancer. 2015 Nov 1;1(3):183-198.

Targeting RAS-mutant cancers: is ERK the key?

Author information

1
Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; mryan4@email.unc.edu.
2
Department of Pharmacology, and the Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; cjder@med.unc.edu.
3
Division of Oncology, Department of Internal Medicine, Alvin J. Siteman Cancer Center, Washington University School of Medicine, ST. Louis, MO 63110, USA; awang@dom.wustl.edu.
4
Departments of Pharmacology and Radiation Oncology, and the Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; adrienne_cox@med.unc.edu.

Abstract

The three RAS genes comprise the most frequently mutated oncogene family in cancer. With significant and compelling evidence that continued function of mutant RAS is required for tumor maintenance, it is widely accepted that effective anti-RAS therapy will have a significant impact on cancer growth and patient survival. However, despite more than three decades of intense research and pharmaceutical industry efforts, a clinically effective anti-RAS drug has yet to be developed. With the recent renewed interest in targeting RAS, exciting and promising progress has been made. In this review, we discuss the prospects and challenges of drugging oncogenic RAS. In particular we focus on new inhibitors of RAS effector signaling and the ERK mitogen-activated protein kinase cascade.

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