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本研究から、ALK、およびROS1融合遺伝子陽性肺がんにおいて、MIG6の欠損がEGFRシグナルの活性化を介してALK、ROS1阻害薬抵抗性に関与する可能性を基礎研究レベルで示し、抗EGFR抗体薬併用による耐性克服の可能性について報告しました。 本文深入解读驱动基因阳性NSCLC的靶向治疗最新进展，涵盖EGFR、ALK、ROS1、MET、HER2、KRAS G12C等靶点，探讨耐药应对、罕见突变治疗突破及新药应用（如德曲妥珠单抗、瑞普替尼等）。 Patients with the less common.
These therapies focus on specific genetic mutations or molecular drivers, such as egfr, alk, ros1, braf, and met, which are commonly implicated in nsclc.
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