Department of Digestive Oncology, University Hospitals Leuven, Herestraat 49, 3000, Leuven, Belgium.
Department of Digestive Oncology, Imelda General Hospital, Bonheiden, Belgium.
Target Oncol. 2020 Jun;15(3):407-410. doi: 10.1007/s11523-020-00727-9.
Current standard-of-care treatment for advanced pancreatic ductal adenocarcinoma is mainly based on conventional cytotoxic chemotherapy. Until recently, no randomized clinical trials had shown any clinically meaningful outcome benefit from targeted therapy in this indication. This is in contrast to many other tumor types. The majority of pancreatic tumors are driven by KRAS mutations, which are generally not amenable to targeted therapy. Driving mutations in the BRAF oncogene have proven to be an interesting molecular target in the management of advanced melanoma and colorectal adenocarcinoma and can be found in 3% of patients with advanced pancreatic ductal adenocarcinoma. Here, we report objective tumor response to treatment with the combination of the BRAF inhibitor vemurafenib and the MEK inhibitor cobimetinib in a patient with poorly differentiated, V600E mutant, advanced pancreatic ductal adenocarcinoma.
目前，晚期胰腺导管腺癌的标准治疗主要基于传统细胞毒性化疗。直到最近，没有随机临床试验显示针对该适应症的靶向治疗具有任何临床意义的获益。这与许多其他肿瘤类型形成鲜明对比。大多数胰腺肿瘤由 KRAS 突变驱动，而这些突变通常不能进行靶向治疗。BRAF 癌基因中的驱动突变已被证明是晚期黑色素瘤和结直肠腺癌治疗中的一个有趣的分子靶点，并且可以在 3%的晚期胰腺导管腺癌患者中发现。在这里，我们报告了一名低分化、V600E 突变的晚期胰腺导管腺癌患者接受 BRAF 抑制剂 vemurafenib 和 MEK 抑制剂 cobimetinib 联合治疗的客观肿瘤反应。
