Ross Andrew L, Sanchez Margaret I, Grichnik James M
Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Dermatol Res Pract. 2011;2011:463184. doi: 10.1155/2011/463184. Epub 2011 Apr 6.
Despite recent advances, the biology underlying nevogenesis remains unclear. Activating mutations in NRAS, HRAS, BRAF, and GNAQ have been identified in benign nevi. Their presence roughly correlates with congenital, Spitz, acquired, and blue nevi, respectively. These mutations are likely to play a critical role in driving nevogenesis. While each mutation is able to activate the MAP kinase pathway, they also interact with a host of different proteins in other pathways. The different melanocytic developmental pathways activated by each mutation cause the cells to migrate, proliferate, and differentiate to different extents within the skin. This causes each mutation to give rise to a characteristic growth pattern. The exact location and differentiation state of the cell of origin for benign moles remains to be discovered. Further research is necessary to fully understand nevus development given that most of the same developmental pathways are also present in melanoma.
尽管最近取得了进展,但痣形成背后的生物学机制仍不清楚。在良性痣中已发现NRAS、HRAS、BRAF和GNAQ的激活突变。它们的存在分别大致与先天性痣、斯皮茨痣、获得性痣和蓝痣相关。这些突变可能在驱动痣形成中起关键作用。虽然每个突变都能够激活丝裂原活化蛋白激酶(MAP)途径,但它们也与其他途径中的许多不同蛋白质相互作用。每个突变激活的不同黑素细胞发育途径导致细胞在皮肤内不同程度地迁移、增殖和分化。这使得每个突变产生一种特征性的生长模式。良性痣的起源细胞的确切位置和分化状态仍有待发现。鉴于大多数相同的发育途径也存在于黑色素瘤中,因此有必要进行进一步研究以充分了解痣的发育。