Journal
CELL REPORTS
Volume 18, Issue 9, Pages 2243-2255Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2017.02.013
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Funding
- Nebraska Cancer and Smoking Disease Research Program (NE DHHS) [LB506 2011-36, LB506 2016-54]
- Public Health Service Grant [R21 CA155175, CA202917]
- UNMC Graduate Studies Office
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Mutant KRAS and c-MYC are oncogenic drivers and rational therapeutic targets for the treatment of pancreatic cancer. Although tumor growth and homeostasis are largely dependent on these oncogenes, a few residual cancer cells are able to survive the ablation of mutant KRAS and c-MYC. By performing a genome-wide gene expression analysis of in vivo-derived bulk tumor cells and residual cancer cells lacking the expression of mutant KRAS or c-MYC, we have identified an increase in autocrine IGF1/AKT signaling as a common survival mechanism in dormant cancer cells. The pharmacological inhibition of IGF-1R reduces residual disease burden and cancer recurrence, suggesting that this molecular pathway is crucial for the survival of cancer cells in the absence of the primary oncogenic drivers.
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