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*

OBJECTIVETo study the clinicopathologic features, differential diagnosis and prognosis of proliferative nodules(PNs) in congenital melanocytic nevi(CMN).

METHODSHistopathologic evaluation and immunohistochemical study by EnVision method were carried out in 8 cases of PNs in CMN. The clinical information and follow-up data were analyzed.

RESULTSThe age of patients ranged from 1 to 54 years (mean 27.6 years). Tumors were located on face (3 cases), on back (2 cases), upper extremities (2 cases) and lower extremities(1 case). Microscopically, PNs with expansile growth were observed in 8 cases of CMN. Melanocytes in PNs show variable pleomorphism with a mitotic activity of 0 to 4 per 10 high power fields. Blending of cells with adjacent CMN was noted in 6 cases. According to the morphology of melanocytes in PNs, it was classified into different types including large oval melanocytes (4 cases), small melanocytes (2 cases) and Spitz-nevus-like forms (2 cases). Immunohistochemically, melanocytes in PNs were consistent with those in adjacent CMN. They were diffusely positive for S-100 protein, but were either negative or focally positive for HMB45. Less than 5% of melanocytes were positive for Ki-67 in 8 cases of PN. Follow-up was available in all cases, ranging from 9 to 82 months. Seven patients with excision of single PN in CMN were alive with no evidence of disease, while 1 patient with multiple PNs in CMN was stable with disease after 62 months follow-up.

CONCLUSIONSPN is a rare melanocytic lesion arising in CMN. Recognition of its specific histologic features can help to avoid being misdiagnosed as melanoma. Long term follow-up should be recommended in patients with PNs, especially in those with atypical histologic features. Further investigation is needed to elucidate its clinical behavior.

Adolescent ; Adult ; Back ; Child ; Child, Preschool ; Diagnosis, Differential ; Extremities ; Facial Neoplasms ; pathology ; Female ; Humans ; Infant ; Male ; Melanocytes ; pathology ; Middle Aged ; Nevus, Pigmented ; pathology ; Prognosis ; Skin Neoplasms ; pathology

Foramen Magnum ; pathology ; Humans ; Male ; Melanocytes ; pathology ; Melanoma ; diagnostic imaging ; pathology ; Meningeal Neoplasms ; diagnostic imaging ; pathology ; Middle Aged ; Radiography ; Skull Neoplasms ; diagnostic imaging ; pathology

Calcitonin ; Carcinoma, Papillary ; drug therapy ; pathology ; surgery ; Female ; Humans ; Melanins ; Melanocytes ; cytology ; pathology ; Middle Aged ; Prognosis ; S100 Proteins ; Thyroid Neoplasms ; drug therapy ; pathology

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

Adolescent ; Adult ; Aged ; Cholesteatoma, Middle Ear ; congenital ; pathology ; Female ; Humans ; Male ; Melanocytes ; Middle Aged ; Young Adult

We reported two cases of clinically typical melasma presenting with unusual histopathologic findings. In one case, the epidermal melanocytes were markedly increased in number and protruded into the dermis, and in the other case, increased epidermal pigmentation as well as dermal melanocytosis were found. We suggested that the various treatment modalities of melasma should be applied depend on its histopathologic finding.
Melanosis/*pathology ; Melanocytes/pathology ; Humans ; Female ; Epidermis/pathology ; Dermis/pathology ; Adult

Both acquired bilateral nevus of Ota-like macules (ABNOM) and nevus of Ota are characterized by the presence of dermal melanocytes. There are no differences in the method of treatment, however, postinflammatory hyperpigmentation (PIH) develops more often in ABNOM than in nevus of Ota following treatment. We investigated the differences in the development of PIH after treatment between ABNOM and nevus of Ota, and the histopathologic differences in the PIH. A total of 82 patients with ABNOM (n=47) and nevus of Ota (n=35) were treated with Q-switched alexandrite laser and followed up 2 weeks and 3 months later. Biopsies were performed on lesional skin before treatment. The distribution and the amount of melanin pigments were visualized with Fontana-Masson stain, and the distribution and the depth of melanocytes were measured by GP-100 (NK1-beteb) stain. Clinically, there was more erythema and PIH in ABNOM than in nevus of Ota. Histopathologically, intradermal melanocytes were clustered in groups and dispersed perivascularly in ABNOM, while melanocytes were scattered evenly throughout the dermis in nevus of Ota. Both groups show that when there is a statistically significant number of melanocytes in the perivascular area, erythema and PIH occur after laser therapy. In conclusion, indirect vessel injury in addition to perivascular clustering melanocytes might be considered the cause of increased PIH after treatment in ABNOM.
Adolescent ; Adult ; Child ; Child, Preschool ; Comparative Study ; Humans ; Hyperpigmentation/*pathology ; Laser Therapy, Low-Level ; Melanocytes/*chemistry/cytology ; Middle Aged ; *Nevus of Ota/pathology/therapy ; *Nevus, Pigmented/pathology/therapy ; Silver Nitrate ; *Skin Neoplasms/pathology/therapy ; Treatment Outcome

Ota's nevus is mongolian spot-like macular blue-black or gray-brown patchy pigmentation that most commonly ocurrs in areas innervated by the first and second division of the trigeminal nerve. Acquired, bilateral nevus of Ota-like macules (ABNOM) is located bilaterally on the face, appears later in life, is blue-brown or slate-gray in color. It is not accompanied by macules on the ocular and mucosal membranes. There is also debate as to whether ABNOM is part of the Ota's nevus spectrum. We report an interesting case of ABNOM associated with Ota's nevus. A 36-yr-old Korean women visited our clinic with dark bluish patch on the right cheek and right conjunctiva since birth. She also had mottled brownish macules on both forehead and both lower eyelids that have developed 3 yr ago. Skin biopsy specimens taken from the right cheek and left forehead all showed scattered, bipolar or irregular melanocytes in the dermis. We diagnosed lesion on the right cheek area as Ota's nevus and those on both forehead and both lower eyelids as ABNOM by clinical and histologic findings. This case may support the view that ABNOM is a separate entity from bilateral Ota's nevus.
Adult ; Biopsy ; Face/pathology ; Female ; Humans ; Melanocytes/cytology ; Nevus of Ota/diagnosis/*pathology ; Nevus, Pigmented/diagnosis/*pathology