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Osimertinib

肿瘤

关键词肿瘤 药物 疾病治疗

词汇介绍

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解析

Osimertinib

       n. 奥斯替尼,阿斯利康非小细胞肺癌新药名

       Osimertinib is an effective third-generation tyrosine kinase inhibitor (TKI) for EGFR-mutant lung cancers. 奥斯替尼是治疗EGFR型肺癌的有效的第三代酪氨酸激酶抑制剂(TKI)。

概述

靶向治疗是精准医疗的重要内容之一,是在分子水平上,针对确定的致癌位点进行定点治疗的方式。目前靶向治疗已经与癌症治疗的三大手段(手术治疗、放射治疗和化疗)并列成为四大治疗手段。肺癌,不管在中国还是在世界上都是发病率和死亡率最高的癌种,其精准医疗研究也是最具有代表性的,不管是在靶向药物的研发还是液体活检应用于肺癌早筛、早诊或者预后方面,在所有癌种中肺癌都堪称典范。从病理类型上肺癌分为非小细胞肺癌、小细胞肺癌等,其中大部分是非小细胞肺癌。所有的癌症从根源上讲都是基因病,在肺癌中重要的驱动突变基因包

Acquired BRAF Rearrangements Induce Secondary Resistance to EGFR therapy in EGFR-Mutated Lung Cancers复制标题

获得性BRAF重排诱导EGFR突变肺癌患者对EGFR治疗的继发性耐药

发表时间:2019-05-01

影响因子:12.5

作者: Morana Vojnic

期刊:J Thorac Oncol

Long-term clinical benefits of EGFR tyrosine kinase inhibitors (EGFR TKIs) in EGFR-mutant NSCLCs remain limited by the development of drug resistance. The most common mechanism of resistance to first- and second-generation EGFR TKIs, the EGFR T790M mutation (which accounts for 60% of cases), can be targeted successfully with third-generation drugs such as osimertinib. Recently, osimertinib has been approved as first-line therapy for EGFR-mutant lung cancer. As expected, disease progression due to acquired resistance to osimertinib has emerged, with the most common alteration described to date being the EGFR C797S mutation. Activation of parallel signaling pathways (amplification of erb-b2 receptor tyrosine kinase 2 gene [HER2] and gene MNNG HOS Transforming gene [MET]) or downstream signaling (mutations in KRAS, phospha-tidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha gene [PIK3CA], and BRAF) has also been shown to induce resistance to osimertinib and other EGFR TKIs. Several acquired gene rearrangements, including fusions involving ALK receptor tyrosine kinase gene (ALK), BRAF, fibroblast growth factor receptor 3 gene (FGFR3), neurotrophic receptor tyrosine kinase 1 gene (NTRK1), and ret proto-oncogene gene (RET), have recently been reported as possible mechanisms of resistance to EGFR TKI therapy.

译文

EGFR酪氨酸激酶抑制剂(EGFR TKIs)在EGFR突变型NSCLC中的长期临床益处仍受限于耐药性的发展。第一代和第二代EGFR TKI最常见的耐药机制,即EGFR T790M突变(占病例的60%),可以成功地用第三代药物如osimertinib进行靶向治疗。最近,osimertinib已被批准作为EGFR突变肺癌的一线治疗药物。正如预期的那样,由于对奥西莫替尼的获得性抗性引起的疾病进展已经出现,迄今为止描述的最常见的改变是EGFR C797S突变。激活平行信号通路(扩增erb-b2受体酪氨酸激酶2基因[HER2]和基因MNNG HOS转化基因[MET])或下游信号(KRAS突变,磷脂酰肌醇-4,5-二磷酸3-激酶催化亚单位α基因[PIK3CA]和BRAF)也被证明可诱导对osimertinib和其他EGFR TKI的耐药。几个获得性基因重排,包括涉及ALK受体酪氨酸激酶基因(ALK),BRAF,成纤维细胞生长因子受体3基因(FGFR3),神经营养受体酪氨酸激酶1基因(NTRK1)和ret原癌基因(RET)的融合,最近报道了作为EGFR TKI治疗耐药的可能机制。