Amphiregulin-mediated EGFR activation drives both intrinsic and acquired resistance to KRAS G12C inhibitors in KRAS G12C-mutant non-small cell lung cancer.

doi:10.1038/s41388-026-03877-8

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Amphiregulin-mediated EGFR activation drives both intrinsic and acquired resistance to KRAS G12C inhibitors in KRAS G12C-mutant non-small cell lung cancer.

Oncogene - 1 Aug 2026

Liu Yifeng, Nanjo Shigeki, Murase Yuya, Arai Sachiko, Watanabe Satoshi, Tsuda Takeshi, Suzuki Junya, Taniguchi Hirokazu, Shibata Kazuhiko, Sato Shigeki, Ueda Tsukasa, Nomura Shunichi, Shimizu Takahiro, Fukuda Koji, Koba Hayato, Kobayashi Takafumi, Tambo Yuichi, Yamamura Kenta, Ohkura Noriyuki, Abo Miki, Hosomichi Kazuyoshi, Yano Seiji

Abstract excerpt

Kirsten rat sarcoma viral oncogene (KRAS) G12C inhibitors have demonstrated clinical efficacy against KRAS G12C-mutant non-small cell lung cancer (NSCLC); however, intrinsic and acquired resistance limit their therapeutic potential. Therefore, combination strategies are needed to address these limitations. While various combination regimens are currently being tested in clinical trials, treatments tailored to...

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Identifiers

PMID: 42393288
DOI: 10.1038/s41388-026-03877-8
PMCID: PMC13407172

Genes

KRAS
AREG
EGFR

Variants

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