No back seat for a progression event-K-RAS as a therapeutic target in CRC.
KRASis the most frequently mutated oncogene in human cancer and plays a central, although poorly understood, role in colorectal cancer (CRC) progression. In this issue ofGenes & 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.
Cancer Research Institute, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.|Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.|Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA.
Emily J
EJ
Poulin
Cancer Research Institute, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.|Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.|Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA.
Kevin M
KM
Haigis
D000818:Animals; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000503:physiopathology*; D004195:Disease Models, Animal; D018450:Disease Progression; D004318:Doxycycline / Q000494:pharmacology; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D011905:Genes, ras / Q000235:genetics*; D015398:Signal Transduction / Q000235:genetics; D016212:Transforming Growth Factor beta / Q000378:metabolism
D016212:Transforming Growth Factor beta; D004318:Doxycycline
Apc; Kras; P53; colorectal cancer; invasion; metastasis