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BRAF Mutation in Colorectal Cancer: An Update: Supplementary Issue: Biomarkers for Colon Cancer

机译:大肠癌中的BRAF突变:更新:补充问题:结肠癌的生物标志物

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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.
机译:大肠癌(CRC)仍然是最致命的癌症相关疾病之一。大约10%的CRC患者的特征是B-Raf原癌基因丝氨酸/苏氨酸激酶(BRAF)基因发生突变,导致残基600(V600E)发生缬氨酸到谷氨酸的变化。超过60%的黑色素瘤患者也存在这种突变。开发了BRAF抑制剂,发现它们可以改善患者的生存率;但是,大多数患者最终都对这些抑制剂产生了抗药性。黑色素瘤患者受益于BRAF抑制剂与有丝分裂原/细胞外信号调节激酶(MEK)抑制剂的组合。不幸的是,结直肠患者的反应效率不高,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,这些发现提高了我们对CRC中BRAF突变生物学的理解。

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