Oncogenic alterations in the BRAF gene are identified in an estimate of 50% of melanomas and cause melanoma development. BRAF kinase inhibitors (BRAFi), including vemurafenib and dabrafenib, were discovered and used in the clinical treatment of BRAF-mutant metastatic melanoma. Though, BRAFi's therapeutic advantages are short term and short-lived associated with drug resistance. Although a few pathways of developed BRAFi resistance have also been established, in approximately 40% of melanomas, the cause for inherited resistance remains unclear. Recognizing a new process of developed BRAFi resistance might provide new possibilities to successfully treat BRAF mutant melanoma. In this study, we are exploring the compensatory alternative pathway followed by BRAFi/MEKi treated resistant cell for maintaining the long-term integrity and survival.

中文翻译：

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侵袭性黑色素瘤型皮肤癌中 BRAF 抑制剂耐药性细胞保护的替代途径。


估计 50% 的黑色素瘤中发现了 BRAF 基因的致癌改变，并导致黑色素瘤的发展。 BRAF 激酶抑制剂 (BRAFi)，包括维莫非尼和达拉非尼，被发现并用于 BRAF 突变型转移性黑色素瘤的临床治疗。然而，BRAFi 的治疗优势是短期的，并且与耐药性相关。尽管已经建立了一些 BRAFi 耐药性的途径，但在大约 40% 的黑色素瘤中，遗传性耐药性的原因仍不清楚。认识到 BRAFi 耐药性的新过程可能为成功治疗 BRAF 突变黑色素瘤提供新的可能性。在这项研究中，我们正在探索 BRAFi/MEKi 处理的耐药细胞所遵循的补偿性替代途径，以维持长期的完整性和存活。