Abstract：
UNASSIGNED: BRAF is a serine-threonine kinase implicated in the regulation of MAPK signaling cascade. BRAF mutation-driven activation occurs in approximately 2-4% of treatment-naive non-small cell carcinomas (NSCLCs). BRAF upregulation is also often observed in tumors with acquired resistance to receptor tyrosine kinase inhibitors (TKIs).
UNASSIGNED: This review describes the spectrum of BRAF mutations and their functional roles, discusses treatment options available for BRAF p.V600 and non-V600 mutated NSCLCs, and identifies some gaps in the current knowledge.
UNASSIGNED: Administration of combined BRAF/MEK inhibitors usually produces significant, although often a short-term, benefit to NSCLC patients with BRAF V600 (class 1) mutations. There are no established treatments for BRAF class 2 (L597, K601, G464, G469A/V/R/S, fusions, etc.) and class 3 (D594, G596, G466, etc.) mutants, which account for up to two thirds of BRAF-driven NSCLCs. Many important issues related to the use of immune therapy for the management of BRAF-mutated NSCLC deserve further investigation. The rare occurrence of BRAF mutations in NSCLC is compensated by high overall incidence of lung cancer disease; therefore, clinical studies on BRAF-associated NSCLC are feasible.
UNASSIGNED: This review describes the spectrum of BRAF mutations and their functional roles, discusses treatment options available for BRAF p.V600 and non-V600 mutated NSCLCs, and identifies some gaps in the current knowledge.
UNASSIGNED: Administration of combined BRAF/MEK inhibitors usually produces significant, although often a short-term, benefit to NSCLC patients with BRAF V600 (class 1) mutations. There are no established treatments for BRAF class 2 (L597, K601, G464, G469A/V/R/S, fusions, etc.) and class 3 (D594, G596, G466, etc.) mutants, which account for up to two thirds of BRAF-driven NSCLCs. Many important issues related to the use of immune therapy for the management of BRAF-mutated NSCLC deserve further investigation. The rare occurrence of BRAF mutations in NSCLC is compensated by high overall incidence of lung cancer disease; therefore, clinical studies on BRAF-associated NSCLC are feasible.
摘要：
■BRAF是一种丝氨酸-苏氨酸激酶，与MAPK信号级联的调节有关。BRAF突变驱动的激活发生在约2-4%的未治疗的非小细胞癌(NSCLCs)中。在对受体酪氨酸激酶抑制剂(TKIs)具有获得性抗性的肿瘤中也经常观察到BRAF上调。
■这篇综述描述了BRAF突变的谱及其功能作用，讨论了BRAFp.V600和非V600突变的NSCLC的治疗选择，并确定当前知识中的一些差距。
■联合使用BRAF/MEK抑制剂通常会产生显着的，虽然通常是短期的，对BRAFV600（1类）突变的非小细胞肺癌患者的益处。没有针对BRAF2类(L597,K601,G464,G469A/V/R/S,融合,等。)和3类(D594、G596、G466等。)突变体，占BRAF驱动的NSCLCs的三分之二。与使用免疫疗法治疗BRAF突变的NSCLC有关的许多重要问题值得进一步研究。在NSCLC中BRAF突变的罕见发生是由肺癌疾病的高总发病率补偿的；因此，BRAF相关NSCLC的临床研究是可行的。
■这篇综述描述了BRAF突变的谱及其功能作用，讨论了BRAFp.V600和非V600突变的NSCLC的治疗选择，并确定当前知识中的一些差距。
■联合使用BRAF/MEK抑制剂通常会产生显着的，虽然通常是短期的，对BRAFV600（1类）突变的非小细胞肺癌患者的益处。没有针对BRAF2类(L597,K601,G464,G469A/V/R/S,融合,等。)和3类(D594、G596、G466等。)突变体，占BRAF驱动的NSCLCs的三分之二。与使用免疫疗法治疗BRAF突变的NSCLC有关的许多重要问题值得进一步研究。在NSCLC中BRAF突变的罕见发生是由肺癌疾病的高总发病率补偿的；因此，BRAF相关NSCLC的临床研究是可行的。
