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Immunoreactivity of α‐melanocyte‐stimulating hormone, adrenocorticotrophic hormone and β‐endorphin in cutaneous malignant melanoma and benign melanocytic naevi
Author(s) -
Michiko Nagahama,
Yoko Funasaka,
M L Fernandez-Frez,
Akiko Ohashi,
Ashok Chakraborty,
Masato Ueda,
Masamitsu Ichihashi
Publication year - 1998
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.1998.02263.x
Subject(s) - medicine , melanoma , melanocyte stimulating hormone , adrenocorticotrophic hormone , beta endorphin , endocrinology , melanocyte , hormone , beta (programming language) , adrenocorticotropic hormone , dermatology , cancer research , computer science , programming language
Melanocyte‐stimulating hormone (MSH) has been reported to enhance the experimental metastatic behaviour of melanoma cells in the mouse model. α‐MSH production and MSH receptor (melanocortin 1 receptor gene) expression have been detected in cultured normal human melanocytes and metastasized melanomas. The exact role of MSH in the metastatic behaviour of human melanoma cells is, however, not yet known. To clarify a possible role of proopiomelanocortin (POMC)‐derived peptides, including α‐MSH, in melanoma development and progression, we analysed immunohistochemically the localization of α‐MSH, adrenocorticotrophic hormone (ACTH) and β‐endorphin in various kinds of benign pigmented naevocytic lesions and malignant melanomas. Three of 21 samples of common and dysplastic naevi showed detectable α‐MSH staining in naevus cells, and five and six of 15 samples were weakly positive for ACTH and β‐endorphin staining, respectively. In melanoma samples, 24 of 45, 23 of 39 and 30 of 42 samples showed positive staining with α‐MSH, ACTH and β‐endorphin antibodies, respectively. Furthermore, staining for all three antibodies was noted to be more intense and diffuse in samples of nodular melanoma, vertically growing acral lentiginous melanoma and superficial spreading melanoma as well as metastatic lesions compared with those of naevi. Although it is yet to be determined whether or not this strong staining for POMC‐derived peptides in advanced melanoma cells indicates a role of autocrine or paracrine regulation, our results suggest a possible involvement of POMC gene products in melanoma progression.