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Genes Dev. 2017 Feb 15;31(4):333-335. doi: 10.1101/gad.297630.117. Epub 2017 Mar 17.

No back seat for a progression event-K-RAS as a therapeutic target in CRC.

Poulin EJ1,2,3, Haigis KM1,2,3.

Author information

1
Cancer Research Institute, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.
2
Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.
3
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA.

Abstract

KRAS is the most frequently mutated oncogene in human cancer and plays a central, although poorly understood, role in colorectal cancer (CRC) progression. In this issue of Genes & Development, Boutin and colleagues (pp. 370-382) present a new mouse model of CRC in which the expression of oncogenic K-RAS is regulated by doxycycline. Using this model, they demonstrate that continued expression of oncogenic K-RAS is required for the survival of primary and metastatic colon cancers and that oncogenic K-RAS activates TGF-β signaling to promote tumor invasion and metastasis.

KEYWORDS:

Apc; Kras; P53; colorectal cancer; invasion; metastasis

PMID:
28314765
PMCID:
PMC5358753
DOI:
10.1101/gad.297630.117
[Indexed for MEDLINE]
Free PMC Article

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