To investigate the role of c-KIT receptor in melanocytic tumour develo
pment and progression, we analysed the expression and localization of
c-KIT by Immunohistochemistry and Western blotting. In contrast to the
positive staining shown by melanocytes and naevus cells in the epider
mis of common naevi (n = 20), all dysplastic naevi (n = 13) were negat
ive, as were dermal melanocytic cells of blue naevi (n = 4) and common
naevi (n = 26). Three out of four superficial spreading melanomas los
t c-KIT expression both in the epidermal and dermal parts, while nodul
ar melanomas showed no expression of c-KIT except in partially positiv
e cells, and six out of seven metastatic melanomas were negative. In a
cral lentiginous melanomas (n = 8), in contrast to other types of mela
noma, all cases with melanoma cells growing basally in the epidermis s
howed strong c-KIT positivity, but melanoma cells growing at the upper
layers of the epidermis and vertically into the dermis lost c-KIT exp
ression. Using the Western blot method on cultured pigment cells, huma
n epidermal melanocytes, junctional naevus cells and one out of three
metastatic melanoma cell lines showed 125 and 145 kDa bands correspond
ing to c-KIT, whereas dermal naevus cells did not. These results sugge
st that dysplastic naevi are distinct from ordinary naevi in terms of
c-KIT expression and that basally growing cells in acral lentigenous m
elanomas could be at an initial stage of tumour progression, before c-
KIT loss occurs.