Melanoma and Immunotherapeutics Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Weill Cornell Medical College, New York, NY 10065, USA.
Human Oncology and Pathogenesis Program, Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA; Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Weill Cornell Medical College, New York, NY 10065, USA.
Cancer Cell. 2014 Nov 10;26(5):603-4. doi: 10.1016/j.ccell.2014.10.017.
In BRAF V600E melanoma patients, RAF inhibitor treatment causes a MEK-inhibitor-sensitive, RAF-inhibitor-resistant adaptive reactivation of ERK signaling. In clinical trials combining MEK and RAF inhibitors, therapeutic efficacy was modestly enhanced, suggesting the utility of inhibiting feedback-reactivated pathways. Strategies for optimally inhibiting ERK signaling should be explored.
在 BRAF V600E 黑色素瘤患者中，RAF 抑制剂治疗会引起 MEK 抑制剂敏感、RAF 抑制剂耐药的 ERK 信号适应性重新激活。在联合使用 MEK 和 RAF 抑制剂的临床试验中，治疗效果略有增强，这表明抑制反馈重新激活的途径具有一定的效用。应探索最佳抑制 ERK 信号的策略。
