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首页> 外文期刊>Journal of Cellular Physiology >The therapeutic potential of targeting the BRAF mutation in patients with colorectal cancer
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The therapeutic potential of targeting the BRAF mutation in patients with colorectal cancer

机译：针对BRAF的治疗潜力结直肠癌患者的突变

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Colorectal cancer is among the most lethal malignancies globally. BRAF is a member of the RAS/RAF/MEK/ERK signaling pathway. Its constitutive activation can result in increased cellular growth, development, invasion, and resistance to therapy. A mutation of the BRAF gene is present in 5–10% of metastatic colorectal cancers. BRAF mutations have been found to predict a lack of benefit to anti‐EGFR therapy in metastatic CRC. Furthermore, CRC containing the BRAF V600E mutation display an innate resistance to BRAF inhibitors. The mechanisms of cell resistance can be explained at least in part by ERK dependent and ERK in‐dependent pathway. Clinical trials evaluating the combinations of BRAF, PI3K, EGFR, and/or MEK inhibitors have revealed promising activity in BRAF mutant containing CRCs. There may be some benefit from future studies that focus on improving the efficacy of combined therapy in CRC with respect to the sustained effects. The aim of current review is to give an overview about the current status and prospective regarding the therapeutic potential of targeting BRAF mutant colorectal cancer.
机译：结直肠癌是最致命的全球恶性肿瘤。RAS /皇家空军/ MEK / ERK信号通路。本构激活可能导致增加细胞生长、发育、入侵和抵抗治疗。基因存在于5 - 10%的转移性大肠癌癌症。预测一个缺乏有利于抗表皮生长因子受体疗法转移性CRC。BRAF V600E突变显示一个天生的阻力BRAF抑制剂。电阻可以至少部分地是由于来解释ERK的依赖和ERK在相关的通路。临床试验评估的组合PI3K BRAF, EGFR和/或MEK抑制剂揭示了BRAF突变承诺活动包含crc。未来的研究,专注于改善联合治疗的疗效在CRC的尊重持续效果。审查是给有关当前概况地位和潜在治疗针对BRAF突变结直肠的潜力癌症。

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