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患者存在 EGFR 突变肺腺癌,出现 BRAF 突变作为获得性耐药机制,对此患者进行 EGFR/BRAF/MEK 联合抑制的肿瘤反应。

Tumor response to EGFR/BRAF/MEK co-inhibition in a patient with EGFR mutated lung adenocarcinoma developing a BRAF mutation as an acquired resistance mechanism.

机构信息

Department of Pulmonology, Cliniques Universitaires Saint-Luc, Avenue Hippocrate 11, 1200 Brussels, Belgium.

Department of Radiology, Cliniques Universitaires Saint-Luc, Avenue Hippocrate 11, 1200 Brussels, Belgium.

出版信息

Lung Cancer. 2021 Sep;159:42-44. doi: 10.1016/j.lungcan.2021.06.025. Epub 2021 Jul 21.

DOI:10.1016/j.lungcan.2021.06.025
PMID:34304052
Abstract

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 mutation as acquired resistance mechanism to osimertinib, who responded favorably to the combination of dabrafenib, trametinib and osimertinib.

摘要

表皮生长因子受体突变型腺癌占高加索人群中未经选择的肺腺癌的 12%和从不吸烟者腺癌的 44%。激活突变,如外显子 19 缺失或外显子 21 Leu858Arg 点突变,可预测肿瘤对表皮生长因子受体酪氨酸激酶抑制剂的反应。不幸的是,通过新的表皮生长因子受体突变、其他基因的突变、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。存在多种可靶向突变的肿瘤的处理尚不清楚。我们报告了一例患者在接受奥希替尼治疗时发生 BRAF 突变作为获得性耐药机制,该患者对 dabrafenib、trametinib 和 osimertinib 的联合治疗反应良好。

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