Department of Clinical Medicine and Surgery, Università Degli Studi di Napoli "Federico II", 80131 Naples, Italy.
Oncology Unit, Ospedale del Mare, 80147 Naples, Italy.
Int J Mol Sci. 2021 Mar 27;22(7):3474. doi: 10.3390/ijms22073474.
As widely acknowledged, 40-50% of all melanoma patients harbour an activating BRAF mutation (mostly BRAF V600E). The identification of the RAS-RAF-MEK-ERK (MAP kinase) signalling pathway and its targeting has represented a valuable milestone for the advanced and, more recently, for the completely resected stage III and IV melanoma therapy management. However, despite progress in BRAF-mutant melanoma treatment, the two different approaches approved so far for metastatic disease, immunotherapy and BRAF+MEK inhibitors, allow a 5-year survival of no more than 60%, and most patients relapse during treatment due to acquired mechanisms of resistance. Deep insight into BRAF gene biology is fundamental to describe the acquired resistance mechanisms (primary and secondary) and to understand the molecular pathways that are now being investigated in preclinical and clinical studies with the aim of improving outcomes in BRAF-mutant patients.
众所周知,40-50%的黑色素瘤患者存在激活的 BRAF 突变(主要是 BRAF V600E)。RAS-RAF-MEK-ERK(MAP 激酶)信号通路的鉴定及其靶向治疗已成为晚期黑色素瘤治疗的重要里程碑,最近也成为完全切除的 III 期和 IV 期黑色素瘤治疗管理的重要里程碑。然而,尽管在 BRAF 突变型黑色素瘤治疗方面取得了进展,但目前批准用于转移性疾病的两种不同方法,免疫疗法和 BRAF+MEK 抑制剂,转移性疾病的 5 年生存率不超过 60%,并且大多数患者在治疗期间因获得性耐药机制而复发。深入了解 BRAF 基因生物学对于描述获得性耐药机制(原发性和继发性)以及理解目前正在进行的分子途径至关重要,这些途径的研究目的是改善 BRAF 突变患者的治疗效果。