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融合作为EGFR突变型非小细胞肺癌对奥希替尼耐药的机制:一例报告及文献综述

Fusion as Resistance Mechanism to Osimertinib in -Mutated NSCLC: A Case Report and Review of Literature.

作者信息

Peroni Marianna, Leonetti Alessandro, Minari Roberta, Verzè Michela, Gnetti Letizia, Bottarelli Lorena, Azzoni Cinzia, Galaverni Marco, Simoni Nicola, Missale Gabriele, Biasini Elisabetta, Tiseo Marcello

机构信息

Department of Medicine and Surgery, University of Parma, Parma, Italy.

Medical Oncology Unit, University Hospital of Parma, Parma, Italy.

出版信息

JTO Clin Res Rep. 2025 Jun 19;6(8):100867. doi: 10.1016/j.jtocrr.2025.100867. eCollection 2025 Aug.

Abstract

Despite the efficacy of osimertinib in the first-line treatment of advanced -mutated NSCLC, the development of resistance is nearly inevitable. mutations and fusions are reported in 1% to 3% of patients with -mutated NSCLC receiving osimertinib and represent potential targetable alterations. In this case report, we discuss the rationale for EGFR-MEK co-inhibition in a patient with -mutated NSCLC treated with osimertinib that developed a fusion at progression. In addition, we provide a brief overview of the current evidence of fusions as an acquired resistance mechanism to osimertinib and potential treatment strategies.

摘要

尽管奥希替尼在一线治疗晚期EGFR突变型非小细胞肺癌(NSCLC)中疗效显著,但耐药的发生几乎不可避免。在接受奥希替尼治疗的EGFR突变型NSCLC患者中,1%至3%的患者报告出现了HER2突变和融合,这些代表了潜在的可靶向改变。在本病例报告中,我们讨论了在一名接受奥希替尼治疗的EGFR突变型NSCLC患者中,其病情进展时出现HER2融合,进行EGFR-MEK联合抑制的理论依据。此外,我们简要概述了目前关于HER2融合作为奥希替尼获得性耐药机制的证据以及潜在的治疗策略。

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