Schulz Alexander, Raetz Jennifer, Karitzky Paula C, Dinter Lisa, Tietze Julia K, Kolbe Isabell, Käubler Theresa, Renner Bertold, Beissert Stefan, Meier Friedegund, Westphal Dana
Department of Dermatology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität (TU) Dresden, Fetscherstrasse 74, 01307 Dresden, Germany.
National Center for Tumor Diseases (NCT), 01307 Dresden, Germany; German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany; Faculty of Medicine and University Hospital Carl Gustav Carus at TU Dresden, 01307 Dresden, Germany; Helmholtz-Zentrum Dresden-Rossendorf (HZDR), 01328 Dresden, Germany.
Cancers (Basel). 2022 Oct 8;14(19):4930. doi: 10.3390/cancers14194930.
BRAFV600 mutations in melanoma are targeted with mutation-specific BRAF inhibitors in combination with MEK inhibitors, which have significantly increased overall survival, but eventually lead to resistance in most cases. Additionally, targeted therapy for patients with NRASmutant melanoma is difficult. Our own studies showed that BRAF inhibitors amplify the effects of MEK inhibitors in NRASmutant melanoma. This study aimed at identifying a BRAF and MEK inhibitor combination with superior anti-tumor activity to the three currently approved combinations. We, thus, assessed anti-proliferative and pro-apoptotic activities of all nine as well as resistance-delaying capabilities of the three approved inhibitor combinations in a head-to-head comparison in vitro. The unconventional combination encorafenib/trametinib displayed the highest activity to suppress proliferation and induce apoptosis, acting in an additive manner in BRAFmutant and in a synergistic manner in NRASmutant melanoma cells. Correlating with current clinical studies of approved inhibitor combinations, encorafenib/binimetinib prolonged the time to resistance most efficiently in BRAFmutant cells. Conversely, NRASmutant cells needed the longest time to establish resistance when treated with dabrafenib/trametinib. Together, our data indicate that the most effective combination might not be currently used in clinical settings and could lead to improved overall responses.
黑色素瘤中的BRAFV600突变可通过针对特定突变的BRAF抑制剂与MEK抑制剂联合治疗,这显著提高了总生存率,但在大多数情况下最终会导致耐药。此外,NRAS突变型黑色素瘤患者的靶向治疗也很困难。我们自己的研究表明,BRAF抑制剂会增强MEK抑制剂对NRAS突变型黑色素瘤的作用。本研究旨在确定一种比目前三种已获批联合用药具有更强抗肿瘤活性的BRAF和MEK抑制剂联合用药方案。因此,我们在体外进行了直接比较,评估了所有九种联合用药的抗增殖和促凋亡活性以及三种已获批抑制剂联合用药的耐药延迟能力。非常规联合用药恩考芬尼/曲美替尼表现出最高的抑制增殖和诱导凋亡活性,在BRAF突变型黑色素瘤细胞中呈相加作用,在NRAS突变型黑色素瘤细胞中呈协同作用。与目前已获批抑制剂联合用药的临床研究结果相关,恩考芬尼/比美替尼在BRAF突变型细胞中最有效地延长了耐药时间。相反,NRAS突变型细胞在用达拉非尼/曲美替尼治疗时建立耐药所需时间最长。总之,我们的数据表明,目前临床应用中可能未使用最有效的联合用药方案,而这可能会改善总体疗效。