BRAF: a driver of the serrated pathway in colon cancer

Anil K Rustgi

doi:10.1016/j.ccr.2013.06.008

BRAF: a driver of the serrated pathway in colon cancer

Cancer Cell. 2013 Jul 8;24(1):1-2. doi: 10.1016/j.ccr.2013.06.008.

Author

Anil K Rustgi¹

Affiliation

¹ Division of Gastroenterology, Departments of Medicine and Genetics, University of Pennsylvania Perelman School of Medicine, 952 BRB, 421 Curie Boulevard, Philadelphia, PA 19104, USA. anil2@mail.med.upenn.edu

PMID: 23845435
DOI: 10.1016/j.ccr.2013.06.008

Abstract

In this issue of Cancer Cell, Rad and colleagues report findings that underscore the importance of oncogenic BRAF mutation coupled with microsatellite instability, p16Ink4a inactivation, and p53 mutation in the serrated pathway of colon cancer development. These findings provide translational insights into potential therapeutic intervention for BRAF mutant colon cancers.

MeSH terms

Colonic Neoplasms / etiology*
Colonic Neoplasms / genetics
Genes, p16
Genes, p53
Humans
Microsatellite Instability
Mutation*
Proto-Oncogene Proteins / genetics
Proto-Oncogene Proteins B-raf / antagonists & inhibitors
Proto-Oncogene Proteins B-raf / genetics*
Proto-Oncogene Proteins p21(ras)
ras Proteins / genetics

Substances

KRAS protein, human
Proto-Oncogene Proteins
BRAF protein, human
Proto-Oncogene Proteins B-raf
Proto-Oncogene Proteins p21(ras)
ras Proteins