Selective Targeting of the KRAS G12C Mutant: Kicking KRAS When It's Down

G Aaron Hobbs; Alfred Wittinghofer; Channing J Der

doi:10.1016/j.ccell.2016.02.015

Selective Targeting of the KRAS G12C Mutant: Kicking KRAS When It's Down

Cancer Cell. 2016 Mar 14;29(3):251-253. doi: 10.1016/j.ccell.2016.02.015.

Authors

G Aaron Hobbs¹, Alfred Wittinghofer², Channing J Der³

Affiliations

¹ Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
² Department of Structural Biology, Max Planck Institute of Molecular Physiology, 44227 Dortmund, Germany.
³ Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Electronic address: cjder@med.unc.edu.

PMID: 26977877
DOI: 10.1016/j.ccell.2016.02.015

Abstract

Two recent studies evaluated a small molecule that specifically binds to and inactivates the KRAS G12C mutant. The new findings argue that the perception that mutant KRAS is persistently frozen in its active GTP-bound form may not be accurate.

Publication types

Review

MeSH terms

Azetidines
Guanosine Diphosphate / metabolism
Guanosine Triphosphate / metabolism
Humans
Mutation / genetics*
Piperazines
Proto-Oncogene Proteins p21(ras) / genetics*
Proto-Oncogene Proteins p21(ras) / metabolism

Substances

ARS853
Azetidines
KRAS protein, human
Piperazines
Guanosine Diphosphate
Guanosine Triphosphate
Proto-Oncogene Proteins p21(ras)

Grants and funding

F32 CA200313/CA/NCI NIH HHS/United States