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Updated: Sep 10, 2025

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
09:38

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

Published on: August 11, 2017

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MED12変異は,炎症性サイトカインによるMEK/ERK経路活性化により,NSCLCにおけるRTK阻害剤耐性を誘発する

Hyun-Min Ryu1,2, Deokhoon Kim3, Jun Young Choi1

  • 1Department of Oncology, Asan Medical Center, University of Ulsan, College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Republic of Korea.

Cellular and molecular life sciences : CMLS
|August 20, 2025
PubMed
まとめ

MED12の変異は,非小細胞肺がん (NSCLC) のレセプターチロシンキナーゼ阻害剤 (RTKI) に対する耐性を引き起こす. トラメチニブでMEK/ ERK経路を標的にすることで,MED12をバイオマーカーとして特定することで,この抵抗を克服できます.

キーワード:
薬剤耐性MED12 変異MEK阻害剤NSCLC についてレセプターチロシンキナーゼ阻害剤

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