黑色素瘤的早期发现对于良好的患者预后至关重要，但我们对早期黑色素瘤发展的机制仍然知之甚少。正常表皮具有良性痣、黑色素瘤和其他皮肤癌中发现的许多序列变异和遗传结构破坏，但仍或多或少地表现正常。一种假设是，在这种情况下，许多黑素细胞具有“肿瘤活性”，但受到周围角质形成细胞提供的微环境的调节，以抑制痣或黑素瘤的进展。有证据表明，从正常皮肤到痣再到黑色素瘤，基因组和表观基因组景观的多项测量中都存在累积紊乱，这可能是促进新生和黑色素瘤发生的关键。版权所有 © 2023 作者。由爱思唯尔公司出版。保留所有权利。

Early detection of melanoma is critical to good patient outcomes, but we still know little about the mechanisms of early melanoma development. Normal epidermis has many of the sequence variants and genetic architecture disruptions found in both benign nevi, melanomas, and other skin cancers, yet continues to behave more or less normally. One hypothesis is that many melanocytes in this context are "tumor competent" but are regulated by the microenvironment provided by the surrounding keratinocytes to inhibit progress to nevi or melanoma. There is evidence of accumulating disorder in several measures of the genomic and epigenomic landscape from normal skin through nevi to melanoma that may be key to promoting nevogenesis and melanomagenesis.Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.