Figure 1.

Melanocytes shift from normal to tumor type. The UV radiation and other mutagen factors generate skin damage and induce mutations in the melanocytes’ DNA. The poor efficacy of the DNA repair mechanism allows mutation accumulation in the DNA and at high tumor mutation burden (TMB) the tumor melanocytes express neoantigens. The tumor site is prone to becoming hypoxic and new blood vessels are created which increases the proinflammatory state in the tumor microenvironment (TME) and promotes tumor cells escape and metastasis. Figure created with Biorender.