braf突变黑色素瘤-哥伦布试验

Q4 Medicine
R. Dummer
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引用次数: 0

摘要

支持:本文的出版未收到任何资助。黑色素瘤是一个重大且日益加重的公共卫生负担,也是皮肤癌相关死亡的最大原因。大约一半的晚期(不可切除或转移)黑色素瘤具有BRAF基因突变,其中V600E是最常见的突变,导致使用BRAF抑制剂进行治疗。然而,单药BRAF抑制剂的反应率很低,因此研究了BRAF和丝裂原激活的细胞外信号调节激酶(MEK)联合抑制。BRAF和MEK抑制剂的靶向治疗与BRAF v600突变黑色素瘤患者的显著长期治疗获益相关,但不良事件发生率增加。encorafenib + binimetinib与vemurafenib或encorafenib在BRAF-突变型黑色素瘤患者中的疗效和安全性(COLUMBUS)试验是一项两部分、随机、开放标签的III期研究,在28个国家的162家医院进行,研究了BRAF抑制剂encorafenib单独或联合MEK抑制剂binimetinib与vemurafenib在晚期BRAF v600 -突变型黑色素瘤患者中的疗效和安全性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
BRAF-mutant Melanoma – The COLUMBUS Trial
Support: No funding was received in the publication of this article. Melanoma represents a significant and increasing public health burden, and is the largest cause of skin cancer-related deaths. Approximately half of advanced (unresectable or metastatic) melanomas have a mutation in the BRAF gene, with V600E being the most common mutation, leading to the therapeutic use of BRAF inhibitors. However, the response rates with single-agent BRAF inhibitors are low, and therefore combined BRAF and mitogen-activated extracellular signal-regulated kinase (MEK) inhibition has been investigated. Targeted therapy with BRAF and MEK inhibitors is associated with significant long-term treatment benefit in patients with BRAF V600-mutated melanoma but has an increased incidence of adverse events. The encorafenib plus binimetinib versus vemurafenib or encorafenib in patients with BRAF-mutant melanoma (COLUMBUS) trial was a two-part, randomised, open-label phase III study conducted at 162 hospitals in 28 countries, and investigated the efficacy and safety of encorafenib, a BRAF inhibitor, alone or in combination with binimetinib, a MEK inhibitor, versus vemurafenib in patients with advanced BRAF V600-mutant melanoma.
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来源期刊
European Oncology and Haematology
European Oncology and Haematology Medicine-Hematology
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