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Article

mTOR inhibitors control the growth of EGFR mutant lung cancer even after acquiring resistance by HGF.

PloS one - 1 Jan 2013

Ishikawa Daisuke, Takeuchi Shinji, Nakagawa Takayuki, Sano Takako, Nakade Junya, Nanjo Shigeki, Yamada Tadaaki, Ebi Hiromichi, Zhao Lu, Yasumoto Kazuo, Nakamura Takahiro, Matsumoto Kunio, Kagamu Hiroshi, Yoshizawa Hirohisa, Yano Seiji

Abstract excerpt

Resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), gefitinib and erlotinib, is a critical problem in the treatment of EGFR mutant lung cancer. Several mechanisms, including bypass signaling by hepatocyte growth factor (HGF)-triggered Met activation, are implicated as mediators of resistance. The mammalian target of rapamycin (mTOR), is a downstream conduit of EGFR and MET...

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Share to Cell Survival
Share to Everolimus

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hepatocyte Growth Factor

Share to Neovascularization, Pathologic

Share to Ribosomal Protein S6 Kinases, 70-kDa

Share to Sirolimus

Share to TOR Serine-Threonine Kinases

Share to Xenograft Model Antitumor Assays

Source

Open in PubMed Open full text

Identifiers

PMID: 23690929
DOI: 10.1371/journal.pone.0062104
PMCID: PMC3653905

Genes

EGFR
HGF
MET

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

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