In un articolo pubblicato online su nature medici del\u00a0Massachusetts General Hospital, Cutaneous Biology Research Center e Cancer Center \u00a0hanno studiato dei topi geneticamente uguali che presentava due geni distinti per il colore scuro della pelle e per il colore rosso \u00a0e hanno attivato un oncogene BRAF in grado di favorire il melanoma. Dopo alcuni mesi met\u00e0 dei topi con cute chiara hanno sviluppato un \u00a0melanoma rispetto a pochi melanomi nei topi con cute scura. Da ci\u00f2 i deduce che potrebbe esserci un altro fattore che favorisce lo sviluppo di melanoma nelle persone rutiliche rispetto alla gi\u00e0 conosciuta fotosensibilit\u00e0<\/p>\n
Leggi l’articolo:\u00a0An ultraviolet-radiation-independent pathway to melanoma carcinogenesis in the red hair\/fair skin background<\/a>:\u00a0<\/strong>People with pale skin, red hair, freckles and an inability to tan|[mdash]|the |[lsquo]|red hair\/fair skin|[rsquo]| phenotype|[mdash]|are at highest risk of developing melanoma, compared to all other pigmentation types1<\/a><\/sup>. Genetically, this phenotype is frequently the product of inactivating polymorphisms in the melanocortin 1 receptor (MC1R<\/em>) gene.\u00a0MC1R<\/em>\u00a0encodes a cyclic AMP-stimulating G-protein-coupled receptor that controls pigment production. Minimal receptor activity, as in red hair\/fair skin polymorphisms, produces the red\/yellow pheomelanin pigment, whereas increasing MC1R activity stimulates the production of black\/brown eumelanin2<\/a><\/sup>. Pheomelanin has weak shielding capacity against ultraviolet radiation relative to eumelanin, and has been shown to amplify ultraviolet-A-induced reactive oxygen species3<\/a>,\u00a04<\/a>,\u00a05<\/a><\/sup>. Several observations, however, complicate the assumption that melanoma risk is completely ultraviolet-radiation-dependent. For example, unlike non-melanoma skin cancers, melanoma is not restricted to sun-exposed skin and ultraviolet radiation signature mutations are infrequently oncogenic drivers6<\/a><\/sup>. Although linkage of melanoma risk to ultraviolet radiation exposure is beyond doubt, ultraviolet-radiation-independent events are likely to have a significant role1<\/a>,\u00a07<\/a><\/sup>. Here we introduce a conditional, melanocyte-targeted allele of the most common melanoma oncoprotein, BRAFV600E<\/sup>, into mice carrying an inactivating mutation in the\u00a0Mc1r<\/em>\u00a0gene (these mice have a phenotype analogous to red hair\/fair skin humans). We observed a high incidence of invasive melanomas without providing additional gene aberrations or ultraviolet radiation exposure. To investigate the mechanism of ultraviolet-radiation-independent carcinogenesis, we introduced an albino allele, which ablates all pigment production on the\u00a0Mc1re\/e<\/sup><\/em>background. Selective absence of pheomelanin synthesis was protective against melanoma development. In addition, normal\u00a0Mc1re\/e<\/sup><\/em>\u00a0mouse skin was found to have significantly greater oxidative DNA and lipid damage than albino-Mc1re\/e<\/sup><\/em>\u00a0mouse skin. These data suggest that the pheomelanin pigment pathway produces ultraviolet-radiation-independent carcinogenic contributions to melanomagenesis by a mechanism of oxidative damage. Although protection from ultraviolet radiation remains important, additional strategies may be required for optimal melanoma prevention.<\/p>\n