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Article

K-Ras mutation-mediated IGF-1-induced feedback ERK activation contributes to the rapalog resistance in pancreatic ductal adenocarcinomas.

Cancer letters - 1 Sept 2012

Wei Feng, Liu Yan, Bellail Anita C, Olson Jeffrey J, Sun Shi-Yong, Lu Guoyue, Ding Lijuan, Yuan Changji, Wang Guangyi, Hao Chunhai

Abstract excerpt

Mammalian target of rapamycin complex 1 (mTORC1) is frequently activated in human cancers; however, clinical trials of rapalog (the mTORC1 inhibitors) have shown that pancreatic ductal adenocarcinomas (PDACs) resist to the treatment. Rapalog treatment activated the extracellular signal-regulated kinase (ERK) pathway in K-Ras mt PDAC cells. K-Ras knockdown abolished the insulin-like growth factor-1 (IGF-1)-induced...

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Identifiers

PMID: 22342683
DOI: 10.1016/j.canlet.2012.02.005
PMCID: PMC3361568

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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