结直肠癌中的BRAF突变:最新进展

Biomarkers in cancer Pub Date : 2015-09-06 eCollection Date: 2015-01-01 DOI:10.4137/BIC.S25248
David Barras
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引用次数: 124

摘要

结直肠癌(CRC)仍然是最致命的癌症相关疾病之一。约10%的结直肠癌患者以B-Raf原癌基因丝氨酸/苏氨酸激酶(BRAF)基因突变为特征,导致残基600 (V600E)处缬氨酸向谷氨酸转变。这种突变也存在于60%以上的黑色素瘤患者中。开发并发现BRAF抑制剂可提高患者生存率;然而,大多数患者最终会对这些抑制剂产生耐药性。黑色素瘤患者受益于BRAF抑制剂与丝裂原/细胞外信号调节激酶(MEK)抑制剂等的联合治疗。不幸的是,结直肠癌患者的反应并不有效,这表明两种癌症类型之间的耐药机制不同。这篇综述旨在阐明最近的发现,以提高我们对CRC中BRAF突变生物学的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
BRAF Mutation in Colorectal Cancer: An Update.

Colorectal cancer (CRC) is still one of the deadliest cancer-related diseases. About 10% of CRC patients are characterized by a mutation in the B-Raf proto-oncogene serine/threonine kinase (BRAF) gene resulting in a valine-to-glutamate change at the residue 600 (V600E). This mutation is also present in more than 60% of melanoma patients. BRAF inhibitors were developed and found to improve patient survival; however, most patients at the end of the track ultimately develop resistance to these inhibitors. Melanoma patients benefit from the combination of BRAF inhibitors with mitogen/extracellular signal-regulated kinase (MEK) inhibitors, among others. Unfortunately, colorectal patients do not respond much efficiently, which suggests different resistance mechanisms between the two cancer types. This review aims at shedding light on recent discoveries that improve our understanding of the BRAF mutation biology in CRC.

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