Papillary cystadenocarcinoma of salivary-glands - an immunohistochemical study.

The immunohistochemical features of 16 cases of papillary cystadenocarcinoma of salivary glands using a panel of monoclonal and polyclonal antibodies were evaluated. The specimens were from patients postoperatively diagnosed as papillary cystadenocarcinoma of salivary glands where the age of the patients ranged from 20-70 years, males were more commonly affected than the females and parotid gland was the most commonly affected site. The cytokeratins detected by MoAb KL1 and K8.12 were positive in all cases showing a heterogeneity in intensity of reaction. A coexpression of vimentin with cytokeratin was found in 10 cases. The tumor cells had a coexpression of S-100 protein and neuron specific enolase (NSE). Glial fibrillary acidic protein (GFAP) was positive in one case with multiple expression of cytokeratins, vimentin NSE, S-100 protein. The polymorphic mucin MAM-6 was positive in all cases and MAM-3 in 8 cases showing different intensity of reaction. The tumor cells were positive for lysozyme (8 cases), lactoferrin (10 cases) and alpha-1-antichymotrypsin (10 cases). The immunoreactive c-erbB-2 oncoprotein on the cell surface membrane was detected in 2 cases. The labeling index of proliferating cell nuclear antigen in the tumor cells ranged from 3.8 to 43.2% (mean 14.2 +/- standard deviation 9.8). Histopathological feature and a heterogeneity of multiple expression of tissue markers may suggest that a population of cells in papillary cystadenocarcinoma may be counterparts of modified myoepithelial cells of pleomorphic adenoma that express epithelial, mesenchymal and neuronal differentiation although the role of myoepithelial cells in the genesis of this tumor is not clear. However, disorganized stratification and malignant transformation of ductal cells may be the most likely possibility in the histogenesis of this tumor.

Immunohistochemical distribution of epithelial membrane antigen in bladder carcinomas as detected with a monoclonal antibody.

Expression of epithelial membrane antigen (EMA) was investigated immunohistochemically in 27 cases of bladder carcinoma using a monoclonal antibody. Normal urothelial epithelium showed EMA staining restricted to the upper layer of the surface epithelium. G-I transitional cell carcinomas demonstrated positive EMA staining which could be divided into the following 3 types; type 1, in which highly stained cells occurred in the upper layer of the neoplastic epithelium; type 2, in which the whole tumour focus was slightly stained; and type 3, in which cells strongly positive for EMA were scattered throughout the tumour focus. G-III (undifferentiated) transitional cell lesions exhibited irregular expression of EMA whereas squamous cell demonstrated specific intense EMA staining within keratinized tumour cells.

Immunohistochemical localization by monoclonal antibody of human epidermal growth factor in mixed tumours of the skin.

Immunohistochemical distribution of human epidermal growth factor (hEGF) was described in 17 cases of mixed tumour of the skin with monoclonal antibody. In normal sweat glands, epithelial cells in the secretory portion and in the transitional area between secretory portion and duct showed prominent staining for hEGF. In the salivary pleomorphic adenoma type of mixed tumour of the skin, luminal tumour cells of tubular and duct-like structures gave a very characteristic hEGF staining reaction. The tumour cells showing strong staining for hEGF were scattered throughout the solid foci in this type of mixed tumour. Tubular epithelial cells in the clear cell adenoma type also displayed a positive hEGF reaction. And apocrine mixed tumours strong staining for hEGF occurred on the apical side of tubular and ductal tumour cells. In view of the immunohistochemical staining patterns for hEGF, the histologic origin of mixed tumours of the skin is suggested to be cells in the secretory portion and those in the transitional portion between secretory portion and duct of the sweat gland.

Immunohistochemical study of carbonic anhydrase in mixed tumours and adenomas of sweat and sebaceous glands.

Immunohistochemical distribution of carbonic anhydrase II (CA) in mixed tumours and adenomas of sweat gland origin and in sebaceous adenomas was demonstrated by the PAP method. Normal sweat glands, both eccrine and apocrine, clear cells of the secretory coils, and ductal epithelial cells all showed conspicuous staining for CA, and sebaceous glands were also positive. Mixed tumours of the skin indicated strongly positive staining for CA in the luminal cells of tubular and duct-like or cystic structures, while most of the other tumour cells were negative. In solid or massive foci, CA positive cells were found scattered among the cellular mass. Sebaceous adenomas were usually moderately positive for CA throughout the tumour.

Expression of keratins during experimentally induced carcinogenesis in hamster cheek pouch visualized polyclonal and monoclonal antibodies.

We obtained immunohistochemical profiles of several keratin proteins during experimentally induced carcinogenesis in hamster cheek-pouch mucosa using a polyclonal antibody (TK; detecting keratins with molecular masses of 41-65 kilodalton) and two monoclonal antibodies (KL1, 55- to 57-kilodalton keratins; PKK1; 40-, 45- and 52.5-kilodalton keratins). The squamous epithelium of normal pouch mucosa exhibited positive TK staining in all layers, KL1 staining in the spinous layer and PKK1 staining in the basal layer, thus indicating a regional or zonal distribution pattern. Epithelia undergoing basal hyperplasia showed irregular localization of PKK1 binding, while hyperkeratinized lesions exhibited the binding pattern found in normal epithelium. In case of epithelial dysplasia, there was reduced KL1 staining in spinous cells and decreased PKK1 staining in the basal and parabasal layers. Papillomas exhibited a rather zonal distribution of keratin staining. All squamous-cell carcinomas, irrespective of their degree of keratinization and infiltration pattern, showed slight or no PKK1 staining. Such lesions were only positive for KL1-detectable keratins in keratinizing tumour cells and exhibited an irregular distribution of TK binding. The expression of keratin proteins during carcinogenesis in hamster cheek-pouch mucosa may parallel that of keratins in human squamous-cell carcinomas originating in the oral mucosa.