Keloids are a common type of pathological scar as a result of skin healing, which are extremely difficult to prevent and treat without recurrence. The pathological mechanism of keloids is the excessive proliferation of fibroblasts, which synthesize more extracellular matrices (ECMs), including type I/III collagen (COL-1/3), mucopolysaccharides, connective tissue growth factor (CTGF, also known as cellular communication network factor 2 (CCN2)), and fibronectin (FN) in scar tissue, mostly through the abnormal activation of transforming growth factor-‍β (TGF-‍β)/Smads pathway (Finnson et al., 2013; Song et al., 2018). Genetic factors, including race and skin tone, are considered to contribute to keloid formation. The reported incidence of keloids in black people is as high as 16%, whereas white people are less affected. The prevalence ratio of colored people to white people is 5:1‍‍-‍‍15:1 (Rockwell et al., 1989; LaRanger et al., 2019). In addition, keloids have not been reported in albinism patients of any race, and those with darker skin in the same race are more likely to develop this disease (LaRanger et al., 2019). Skin melanocyte activity is significantly different among people with different skin tones. The more active the melanocyte function, the more melanin is produced and the darker the skin. Similarly, in the same individual, the incidence of keloids increases during periods when melanocytes are active, such as adolescence and pregnancy. Keloids rarely appear in areas where melanocytes synthesize less melanin, such as in the palms and soles. Thus, the formation of keloids seems to be closely related to melanocyte activity.
Adolescent ; Cells, Cultured ; Exosomes/metabolism* ; Fibroblasts/metabolism* ; Humans ; Keloid/pathology* ; Melanins/metabolism* ; Melanocytes/pathology* ; Pilot Projects ; Skin/metabolism* ; Transforming Growth Factor beta/metabolism*

Stasis dermatitis is an itchy, scaly, and hyperpigmented condition of the lower leg due to venous insufficiency. Hemosiderin and/or melanin have been considered responsible for the brown pigmentation. However, there are not sufficient histopathologic studies. In this retrospective study the hospital records and biopsy slides of 20 patients were reviewed to determine the pathogenetic mechanisms of brown pigmentation in stasis dermatitis. Fifteen were men (75%) and 5 were women (25%) with a mean age of 46.2+/-8.2 yr (18-76), mean age at onset of 43.4+/-18.0 yr (17-73), and a mean duration of the disease 2.8+/-2.5 yr (0.25-10). All patients had varicose vein and complained of pruritus. On histopathologic evaluation, two cases out of 20 (3 skin biopsy specimens from 25 samples) showed dermal melanocytes containing melanin, and incontinence of melanin pigment was observed in 5 cases, which indicates that melanin pigments from epidermis could contribute to cutaneous pigmentation in stasis dermatitis. However, the existence of dermal melanocytes in two cases cannot be explained because normally the dermis contains no melanocytes. Further studies concerning the role of iron or inflammatory cytokines on the development of dermal melanocytes should be conducted.
Adolescent ; Adult ; Aged ; Dermatitis/etiology/metabolism/*pathology ; Dermis/metabolism/pathology ; Female ; Humans ; Hyperpigmentation/etiology/metabolism/*pathology ; Leg Dermatoses/etiology/metabolism/pathology ; Male ; Melanins/metabolism ; Melanocytes/metabolism/*pathology ; Middle Aged ; Venous Insufficiency/complications

Adult ; Diagnosis, Differential ; Humans ; MART-1 Antigen ; metabolism ; Magnetic Resonance Imaging ; Male ; Medulloblastoma ; metabolism ; pathology ; Melanocytes ; pathology ; Melanoma ; diagnosis ; metabolism ; pathology ; surgery ; Melanoma-Specific Antigens ; metabolism ; Meningeal Neoplasms ; diagnosis ; metabolism ; pathology ; surgery ; Neoplasms, Multiple Primary ; diagnosis ; metabolism ; pathology ; surgery ; Neurilemmoma ; metabolism ; pathology ; Nevus of Ota ; diagnosis ; metabolism ; pathology ; surgery ; S100 Proteins ; metabolism ; Skin Neoplasms ; diagnosis ; metabolism ; pathology ; surgery ; Vimentin ; metabolism

The increasing incidence and mortality associated with advanced stages of melanoma are cause for concern. Few treatment options are available for advanced melanoma and the 5-year survival rate is less than 15%. Targeted therapies may revolutionize melanoma treatment by providing less toxic and more effective strategies. However, maximizing effectiveness requires further understanding of the molecular alterations that drive tumor formation, progression, and maintenance, as well as elucidating the mechanisms of resistance. Several different genetic alterations identified in human melanoma have been recapitulated in mice. This review outlines recent progress made in the development of mouse models of melanoma and summarizes what these findings reveal about the human disease. We begin with a discussion of traditional models and conclude with the recently developed RCAS/TVA somatic cell gene delivery mouse model of melanoma.
9,10-Dimethyl-1,2-benzanthracene ; Animals ; Avian Leukosis Virus ; genetics ; Avian Proteins ; genetics ; metabolism ; Cell Line, Tumor ; Disease Models, Animal ; Gene Transfer Techniques ; Genetic Vectors ; genetics ; Humans ; Melanocytes ; metabolism ; Melanoma ; genetics ; pathology ; Melanoma, Experimental ; chemically induced ; genetics ; Mice ; Mice, Transgenic ; Neoplasm Transplantation ; Receptors, Virus ; genetics ; metabolism ; Skin Neoplasms ; genetics ; pathology ; Tetradecanoylphorbol Acetate ; Transgenes