| First Author | Eser S | Year | 2013 |
| Journal | Cancer Cell | Volume | 23 |
| Issue | 3 | Pages | 406-20 |
| PubMed ID | 23453624 | Mgi Jnum | J:197054 |
| Mgi Id | MGI:5490703 | Doi | 10.1016/j.ccr.2013.01.023 |
| Citation | Eser S, et al. (2013) Selective requirement of PI3K/PDK1 signaling for Kras oncogene-driven pancreatic cell plasticity and cancer. Cancer Cell 23(3):406-20 |
| abstractText | Oncogenic Kras activates a plethora of signaling pathways, but our understanding of critical Ras effectors is still very limited. We show that cell-autonomous phosphoinositide 3-kinase (PI3K) and 3-phosphoinositide-dependent protein kinase 1 (PDK1), but not Craf, are key effectors of oncogenic Kras in the pancreas, mediating cell plasticity, acinar-to-ductal metaplasia (ADM), and pancreatic ductal adenocarcinoma (PDAC) formation. This contrasts with Kras-driven non-small cell lung cancer, where signaling via Craf, but not PDK1, is an essential tumor-initiating event. These in vivo genetic studies together with pharmacologic treatment studies in models of human ADM and PDAC demonstrate tissue-specific differences of oncogenic Kras signaling and define PI3K/PDK1 as a suitable target for therapeutic intervention specifically in PDAC. |
