Functional dissection of the KRAS G12C mutation by comparison among multiple oncogenic driver mutations in a lung cancer cell line model

Keigo Kobayashi, Hideki Terai, Hiroyuki Yasuda, Junko Hamamoto, Yuichiro Hayashi, Osamu Takeuchi, Yoichiro Mitsuishi, Keita Masuzawa, Tadashi Manabe, Shinnosuke Ikemura, Ichiro Kawada, Yukio Suzuki, Kenzo Soejima, Koichi Fukunaga

研究成果: Article査読

抄録

The development of molecular targeted therapy has improved clinical outcomes in patients with life-threatening advanced lung cancers with driver oncogenes. However, selective treatment for KRAS-mutant lung cancer remains underdeveloped. We have successfully characterised specific molecular and pathological features of KRAS-mutant lung cancer utilising newly developed cell line models that can elucidate the differences in driver oncogenes among tissues with identical genetic backgrounds. Among these KRAS-mutation-associated specific features, we focused on the IGF2-IGF1R pathway, which has been implicated in the drug resistance mechanisms to AMG 510, a recently developed selective inhibitor of KRAS G12C lung cancer. Experimental data derived from our cell line model can be used as a tool for clinical treatment strategy development through understanding of the biology of lung cancer. The model developed in this paper may help understand the mechanism of anticancer drug resistance in KRAS-mutated lung cancer and help develop new targeted therapies to treat patients with this disease.

本文言語English
ページ(範囲)1-7
ページ数7
ジャーナルBiochemical and Biophysical Research Communications
534
DOI
出版ステータスPublished - 2021 1 1

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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