EGFR-mutant adenocarcinomas represent 12% of unselected lung adenocarcinomas and 44% of never smoker adenocarcinomas in the Caucasian population. Activating mutations like exon19 deletion or exon21 Leu858Arg point mutations are predictive of tumor response to EGFR tyrosine kinase inhibitors. Unfortunately, acquired resistance inevitably occurs by the development of novel EGFR mutations, mutations in other genes, gene amplification, gene fusion or tumor transformation. The management of tumors presenting multiple targetable mutations is unclear. We present the case of a patient developing a BRAF^V600 mutation as acquired resistance mechanism to osimertinib, who responded favorably to the combination of dabrafenib, trametinib and osimertinib.

在白种人人群中，EGFR 突变型腺癌占未选择的肺腺癌的 12% 和从不吸烟的腺癌的 44%。激活突变如外显子 19 缺失或外显子 21 Leu858Arg 点突变可预测肿瘤对 EGFR 酪氨酸激酶抑制剂的反应。不幸的是，新的 EGFR 突变、其他基因突变、基因扩增、基因融合或肿瘤转化的发展不可避免地会发生获得性耐药。存在多个可靶向突变的肿瘤的管理尚不清楚。我们介绍了一名患者发生 BRAF ^V600突变作为对奥希替尼的获得性耐药机制，该患者对达拉非尼、曲美替尼和奥希替尼的组合反应良好。