BRAF融合作为egfr突变的非小细胞肺癌对奥西替尼的耐药机制：一例报告和文献综述

IF 3 Q2 ONCOLOGY

JTO Clinical and Research Reports Pub Date : 2025-06-19 DOI:10.1016/j.jtocrr.2025.100867

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

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引用次数: 0

摘要

尽管奥西替尼在一线治疗晚期egfr突变的NSCLC有疗效，但耐药的发展几乎是不可避免的。在接受奥西替尼治疗的egfr突变NSCLC患者中，有1%至3%的患者报告了BRAF突变和融合，这代表了潜在的靶向改变。在本病例报告中，我们讨论了在接受奥西替尼治疗的egfr突变NSCLC患者中发生CTNNA1-BRAF融合的EGFR-MEK共抑制的基本原理。此外，我们简要概述了BRAF融合作为对奥西替尼的获得性耐药机制和潜在治疗策略的现有证据。

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

Despite the efficacy of osimertinib in the first-line treatment of advanced EGFR-mutated NSCLC, the development of resistance is nearly inevitable. BRAF mutations and fusions are reported in 1% to 3% of patients with EGFR-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 EGFR-mutated NSCLC treated with osimertinib that developed a CTNNA1-BRAF fusion at progression. In addition, we provide a brief overview of the current evidence of BRAF fusions as an acquired resistance mechanism to osimertinib and potential treatment strategies.

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