The likelihood of heterogeneity or additional mutation in KRAS or associated oncogenes to compromise targeting of oncogenic KRAS G12C
V. L. Cannataro, S. G. Gaffney, C. Stender, Z.-M. Zhao, M. Philips, A. Greenstein, J. P. Townsend
The study finds no evidence of resistance-conferring mutations in KRAS or downstream genes in KRAS G12C positive tumors at treatment time, and predicts BRAF mutations as likely resistance mechanisms with existing therapies.
bioRxiv · Jun 13, 2017Cancer Biology