Identification of signals involved melanomagenesis and melanoma growth, expecially, UV-induced melanoma formation

皮肤白皙、头发红的白种人更容易患紫外线诱发的黑色素瘤。我们制造了含有不同种类黑色素的表皮黑色素细胞的黑色素瘤模型小鼠，然后用UVB或UVA照射。然而，UVA照射不会加速黑色素瘤的形成，而UVB则会。尤其是白种人分泌更多的现象胺。UVB照射后，含黑色素的表皮CPDs延长。DNA修复缺陷小鼠也显示出早期黑色素瘤形成。这些结果表明，由UVB和黑色素引起的DNA损伤可能是黑色素瘤形成的触发因素。

Fair skin caucasians with red hair are more susceptible to UV-induced melanoma. We generated melanoma model mouse harboring epidermal melanocytes with different melanin species, then irradiated with UVB or UVA. UVA irradiation did not accelerate melanoma formation, however, UVB did so. Especially, pheomlanin, which is produced more in caucasians. Pheomelanin containing epidermis showed prolonged CPDs after UVB irradiation. DNA repair-deficient mouse also showed early melanoma formation. These results indicate that DNA damages caused by UVB and pheomelanin could be a trigger of melanoma formation.