RESUMO
The relationship between skin color and skin cancer is well established: the less melanin in one's skin the greater the risk for developing skin cancer. This review is in two parts. First, we summarize the current understanding of the cutaneous pigmentary system and trace melanin from its synthesis in the pigment cell melanosomes through its transfer to keratinocytes. We also present new methods for reducing melanin content in hyper-pigmented areas of skin such as solar lentigenes, melasma, and post-inflammatory hyperpigmentation. Second, we present evidence that at least one mechanism for the development of metastatic melanoma and other solid tumors is fusion and hybridization of leucocytes such as macrophages with primary tumor cells. In this scenario, hybrid cells express both the chemotactic motility of the leucocyte and the de-regulated cell division of the tumor cell, causing the cells to migrate a deadly journey to lymph nodes, distant organs, and tissues.
Assuntos
Hiperpigmentação , Melaninas/metabolismo , Neoplasias Cutâneas , Pigmentação da Pele/fisiologia , Humanos , Hiperpigmentação/metabolismo , Hiperpigmentação/patologia , Neoplasias Cutâneas/metabolismo , Neoplasias Cutâneas/patologia , Neoplasias Cutâneas/prevenção & controleRESUMO
A review of the basics of pigment cell biology is followed by a discussion of the characteristics of several disorders of hypopigmentation. By determining such features as inheritance pattern, time of onset (congenital, childhood, adulthood), natural history (stable vs progressive), type of pigment loss (diffuse or circumscribed), distribution of lesions (generalized vs localized), degree of pigment loss (incomplete or complete), number of melanocytes, if any, in biopsy specimens of affected areas, type of melanocytic dysfunction, and associated inflammation or infection, one can classify the disorders of hypopigmentation. The proposed pathophysiology for each disorder of hypomelanosis is presented.