Estrogen Receptor β in Melanoma: From Molecular Insights to Potential Clinical Utility.

摘要: Cutaneous melanoma is an aggressive tumor with its incidence increasing faster than any other cancer in the past decades. Melanoma a heterogeneous tumor, most patients harboring mutations BRAF or NRAS oncogenes, leading to overactivation of MAPK/ERK and PI3K/Akt pathways. The current therapeutic approaches are based on therapies targeting mutated downstream pathway, monoclonal antibodies against immune checkpoint blockade. However, treatment resistance side effects common events these strategies. Increasing evidence supports that hormone-related cancer. higher males females have significant survival advantage over men. Estrogens exert their through estrogen receptors (ER ERβ) opposite growth: ER associated proliferative action ERβ anticancer effect. predominant receptor expression decreases progression, supporting role as suppressor. Thus, now considered effective molecular target for treatment. 17β-estradiol was reported inhibit cells proliferation. clinical trials did not provide expected benefits. In vitro studies demonstrate ligands proliferation (but BRAF) mutation, suggesting activation might impair development inhibition pathway. These data suggest agonists be strategy, combination MAPK inhibitors, mutant melanomas. era personalized medicine, pretreatment evaluation ER isoforms together concurrent oncogenic should before selecting appropriate intervention. Natural compounds specifically bind been identified. phytoestrogens decrease cells. Importantly, unrelated melanomas, that, addition activating function, additional mechanisms. A better identification will help increase options this pathology.