Janowska Agata, Iannone Michela, Fidanzi Cristian, Romanelli Marco, Filippi Luca, Del Re Marzia, Martins Manuella, Dini Valentina
Unit of Dermatology, University of Pisa, 56126 Pisa, Italy.
Unit of Neonatology, University of Pisa, 56126 Pisa, Italy.
Cancers (Basel). 2022 Apr 23;14(9):2104. doi: 10.3390/cancers14092104.
Immune dysregulation, in combination with genetic and epigenetic alterations, induces an excessive proliferation of uncontrolled melanoma cells followed by dissemination of the tumor cells to distant sites, invading organs and creating metastasis. Although immunotherapy, checkpoint inhibitors and molecular targeted therapies have been developed as treatment options for advanced melanoma, there are specific mechanisms by which cancer cells can escape treatment. One of the main factors associated with reduced response to therapy is the ability of residual tumor cells to persist in a dormant state, without proliferation. This comprehensive review aimed at understanding the genetic basis of dormancy/awakening phenomenon in metastatic melanoma will help identify the possible therapeutical strategies that might eliminate melanoma circulating tumor cells (CTCs) or keep them in the dormant state forever, thereby repressing tumor relapse and metastatic spread.
免疫失调与基因和表观遗传改变相结合，会诱导不受控制的黑色素瘤细胞过度增殖，随后肿瘤细胞扩散到远处部位，侵入器官并形成转移。尽管免疫疗法、检查点抑制剂和分子靶向疗法已被开发作为晚期黑色素瘤的治疗选择，但癌细胞仍有特定机制可逃避治疗。与治疗反应降低相关的主要因素之一是残留肿瘤细胞保持休眠状态而不增殖的能力。这篇旨在了解转移性黑色素瘤休眠/唤醒现象遗传基础的综述，将有助于确定可能消除黑色素瘤循环肿瘤细胞（CTC）或使其永远保持休眠状态的治疗策略，从而抑制肿瘤复发和转移扩散。
