Gracia-Hernandez Maria, Munoz Zuleima, Villagra Alejandro
Department of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, The George Washington University, Washington, DC 20052, USA.
Cancers (Basel). 2021 Dec 8;13(24):6180. doi: 10.3390/cancers13246180.
Melanoma is the least common but deadliest type of skin cancer. Melanomagenesis is driven by a series of mutations and epigenetic alterations in oncogenes and tumor suppressor genes that allow melanomas to grow, evolve, and metastasize. Epigenetic alterations can also lead to immune evasion and development of resistance to therapies. Although the standard of care for melanoma patients includes surgery, targeted therapies, and immune checkpoint blockade, other therapeutic approaches like radiation therapy, chemotherapy, and immune cell-based therapies are used for patients with advanced disease or unresponsive to the conventional first-line therapies. Targeted therapies such as the use of BRAF and MEK inhibitors and immune checkpoint inhibitors such as anti-PD-1 and anti-CTLA4 only improve the survival of a small subset of patients. Thus, there is an urgent need to identify alternative standalone or combinatorial therapies. Epigenetic modifiers have gained attention as therapeutic targets as they modulate multiple cellular and immune-related processes. Due to melanoma's susceptibility to extrinsic factors and reversible nature, epigenetic drugs are investigated as a therapeutic avenue and as adjuvants for targeted therapies and immune checkpoint inhibitors, as they can sensitize and/or reverse resistance to these therapies, thus enhancing their therapeutic efficacy. This review gives an overview of the role of epigenetic changes in melanoma progression and resistance. In addition, we evaluate the latest advances in preclinical and clinical research studying combinatorial therapies and discuss the use of epigenetic drugs such as HDAC and DNMT inhibitors as potential adjuvants for melanoma patients.
黑色素瘤是最不常见但最致命的皮肤癌类型。黑色素瘤的发生是由一系列致癌基因和肿瘤抑制基因的突变及表观遗传改变驱动的,这些改变使得黑色素瘤得以生长、演变和转移。表观遗传改变还可导致免疫逃逸和对治疗产生耐药性。尽管黑色素瘤患者的标准治疗包括手术、靶向治疗和免疫检查点阻断,但对于晚期疾病患者或对传统一线治疗无反应的患者,也会使用其他治疗方法,如放射治疗、化疗和基于免疫细胞的治疗。使用BRAF和MEK抑制剂等靶向治疗以及抗PD-1和抗CTLA4等免疫检查点抑制剂仅能改善一小部分患者的生存率。因此,迫切需要确定替代的单一疗法或联合疗法。表观遗传修饰剂作为治疗靶点已受到关注,因为它们可调节多个细胞和免疫相关过程。由于黑色素瘤对外在因素敏感且具有可逆性,表观遗传药物正作为一种治疗途径以及靶向治疗和免疫检查点抑制剂的佐剂进行研究,因为它们可使黑色素瘤对这些治疗敏感和/或逆转耐药性,从而提高其治疗效果。本综述概述了表观遗传变化在黑色素瘤进展和耐药中的作用。此外,我们评估了研究联合疗法的临床前和临床研究的最新进展,并讨论了使用组蛋白去乙酰化酶(HDAC)和DNA甲基转移酶(DNMT)抑制剂等表观遗传药物作为黑色素瘤患者潜在佐剂的情况。