| First Author | Rajbhandari N | Year | 2017 |
| Journal | Cell Rep | Volume | 18 |
| Issue | 9 | Pages | 2243-2255 |
| PubMed ID | 28249168 | Mgi Jnum | J:256196 |
| Mgi Id | MGI:6103218 | Doi | 10.1016/j.celrep.2017.02.013 |
| Citation | Rajbhandari N, et al. (2017) Autocrine IGF1 Signaling Mediates Pancreatic Tumor Cell Dormancy in the Absence of Oncogenic Drivers. Cell Rep 18(9):2243-2255 |
| abstractText | 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. |
