[Immunohistological investigation of the histological origin and differentiation of pleomorphic adenoma of the parotid gland].
Immunohistological expressions of the cytokeratin (CK) subclass, vimentin, glial fibral antigen protein (GFAP), alpha-smooth muscle actin, and S-100 protein were investigated in pleomorphic adenoma of the parotid gland. In addition, the correlation between immunohistological findings in the normal parotid gland and those in pleomorphic adenoma was examined. Vimentin, S-100 protein, and GFAP, which were not detected in the normal parotid gland, were observed in pleomorphic adenoma. Only CK-1, which was not detected in the normal parotid gland, was expressed intensely in squamous metaplastic lesions of pleomorphic adenoma. All other CK detected in pleomorphic adenoma were also expressed in the normal parotid gland. Therefore, the expression of vimentin, S-100 protein, GFAP, and CK-1 in pleomorphic adenoma is related to oncogenesis. Since most types of CK expression were observed in solid pleomorphic adenoma lesions and all types of CK expression detected in other lesions were included, cellular differentiation between solid and nonsolid lesions was elucidated. According to the pattern of CK subclass expression, the following sequence of differentiation was suggested; solid lesion-->myxoid lesion-->chondroid lesion, solid lesion-->tubular lesion, solid lesion-->myoepithelioid lesion, and solid lesion-->squamous metaplastic lesion. In normal parotid glands, satellite cells around the ductal cells showed all types of CK subclass expression detected in myoepithelial cells, acinus cells, and ductal cells. Since the types and patterns of CK expression in solid lesions of pleomorphic adenoma are the same as those in satellite cells in the normal parotid gland, pleomorphic adenoma seems to originate from satellite cells. If satellite cells in the normal parotid gland are considered to be so-called reserve cells in the bicellular theory, the origin and cellular differentiation of pleomorphic adenoma can be explained in relation to CK subclass expression.
Murakami
M
M
Department of Otolaryngology, Kyoto Prefectural University of Medicine.
Makino
I
I
Nin
F
F
Nishiyama
Y
Y
Saitou
Y
Y
Murakami
Y
Y
D000199:Actins / Q000378:metabolism; D008949:Adenoma, Pleomorphic / Q000378:metabolism / Q000473:pathology*; D002454:Cell Differentiation; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D007633:Keratins / Q000378:metabolism; D010306:Parotid Gland / Q000378:metabolism / Q000473:pathology; D010307:Parotid Neoplasms / Q000378:metabolism / Q000473:pathology*; D009418:S100 Proteins / Q000378:metabolism; D014746:Vimentin / Q000378:metabolism
D000199:Actins; D005904:Glial Fibrillary Acidic Protein; D009418:S100 Proteins; D014746:Vimentin; D007633:Keratins