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Results for “SALIVARY GLAND NEOPLASMS”
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Sialadenoma papilliferum: report of case and review of literature.
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Acinic cell adenocarcinoma of a minor salivary gland: report of a case.
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Acinic cell adenocarcinoma arising from minor salivary gland tissue.
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Adenomatoid hyperplasia of the palate in an Asian child.
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Red-blue lesion of the hard palate.
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Basaloid monomorphic adenoma presenting as an expanding buccal mass: a case report.
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Immunocytochemical detection of carcinoembryonic antigen in salivary gland tumors.
The immunoperoxidase method was applied for carcinoembryonic antigen (CEA) detection in biopsy specimens of salivary gland tumors. 9 out of 10 adenoidcystic carcinomas revealed a strong and abundant reaction in tumoral glands. 10 other specimens of pleomorphic adenomas showed weak staining in the areas of epithelial proliferation. Normal glands adjacent to the tumor mass revealed a weak but constant reaction on the luminal border. As in other types of gland tumor, the quantitative estimation of CEA production by salivary gland tumors may be useful in the monitoring of recurrencies.
Pleomorphic adenoma of the buccal gland in a child.
The rare case of a 9-year-old Japanese girl with pleomorphic adenoma of the buccal mucosa is described. We review the literature of pleomorphic adenoma in children.
Intra-oral benign solid oncocytoma.
Oncocytomas are extremely uncommon in the intra-oral minor salivary glands, they are rarely reported in the literature and the histopathology and clinical details are inadequately documented. This has led to uncertainty with regard to the behaviour and prognosis of this type of lesion. A case of benign solid oncocytoma arising from intra-oral minor salivary glands is reported here with a brief review of the pertinent literature.
Papillary cystic adenocarcinoma of minor salivary glands.
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Pleomorphic adenoma of the cheek.
The mucosa of the cheek is a relatively rare site of occurrence for intraoral pleomorphic adenoma. A case of a large pleomorphic adenoma of the cheek is reported and a review of this lesion in the cheek is presented.
Distribution of the VLA family of integrins in normal salivary gland and in pleomorphic adenoma.
The extracellular matrix (ECM) and the alterations in tumour stroma affect the biologic behaviour of tumours. These interactions are, at least in part, mediated by the integrin superfamily. In this study we examined the immunohistochemical expression of the "very late activation" (VLA)-integrins in pleomorphic adenomas and in the corresponding normal tissues. Normal salivary gland expresses integrins in the myoepithelial cells (MEC) and in the basal and dark cells of ducts. This pattern is retained in pleomorphic adenoma. Regardless of the straining intensity, these tumour cells have a VLA expression similar to normal basal and dark cells, with only a few cells bearing MEC characteristics. We suggest that the tumour cells of pleomorphic adenoma have a common origin but show different stages of differentiation. Only cells bearing basement membrane (BM)-associated material form typical tubulo-ductal structures.
The expression of different intermediate-sized filaments in human salivary glands and their tumours.
The intermediate-sized filaments can be divided into several groups which are characteristic of different types of tissues (e.g.: epithelial, mesenchymal, muscle, astrocytic and neural origin). Antibodies specific for some of these filament types have been used to analyse a group of salivary gland tumours. Prekeratin-positive cells were seen in the normal gland, cystadenolymphomas, mucoepidermoid tumours, and squamous cell carcinomas which are all tumours of epithelial origin. The pleomorphic adenomas showed the presence of some cells which appeared to contain both prekeratin and vimentin. The results are discussed with respect to their histogenetic implications.
Basal membrane associated substances in human salivary glands and salivary gland tumours.
Human salivary gland tissue was analysed with respect to the distribution of basal membrane associated substances. Collagen type IV and laminin were studied on the basis of monoclonal antibodies, fibronectin was analysed with polyclonal antibodies. The structure of the basal membrane was well preserved in normal salivary gland tissue. There was a continuous staining of the basal membrane around the acini and the ducts. The labelling for these substances appeared to be associated with the myoepithelial cells. Pleomorphic adenomas exhibited a heterogeneous pattern for the basal membrane substances. Focally, there was an augmentation of collagen IV and laminin, as well as of fibronectin. This was observed in the neighbourhood of myoepithelial like cells. Other parts of pleomorphic adenomas showed an interruption of the basal membrane. Adenoid cystic carcinomas displayed a clear staining of the basal membrane associated substances in the pseudocysts. Stromal trabeculae were stained in an irregular manner. Acinic cell tumours, adenocarcinomas, mucoepidermoid tumours and squamous cell carcinomas (for comparison taken from other regions in the head and neck area) presented a clear destruction of the basal membrane as visualized by antibodies against collagen IV and laminin. The study of the basal membrane substances may be helpful for identifying special features of salivary gland tumours and for grading the amount of invasive behaviour in the malignant tumours.
Heterogeneity of keratin expression in epithelial tumor cells of adenolymphoma in paraffin sections.
Immunohistochemical expressions of keratin polypeptides detected by monoclonal antibodies were described in tumor cells of adenolymphoma, and the possibility of intercalated duct and ductal basal cells in the salivary glands being the progenitors was discussed. Basal cells in the tumor showed positive staining for keratin nos. 8, 13, 16, 18 and 19 detecting for monoclonal keratin antibodies (PKK 1, K 4.62, K 8.12, K 8.13), columnar tumor cells displayed strongly positive reactions with RPN 1164 and K4.62 suggesting keratin nos. 8 and 19. Great heterogeneity of distribution for keratin polypeptides was displayed by epithelial cells of adenolymphoma. Intercalated duct cells of normal salivary glands reacted with RPN 1164, RPN 1165, K 4.62 and K 8.13 monoclonal antibodies, which indicates the presence of keratins 8 and 19; and ductal basal cells reacted with PKK 1, K 4.62 and K 8.12, suggesting nos. 8, 13, 16, 18 and 19 keratins. Distribution of involucrin was variable in tumor epithelium of adenolymphoma, and was negative in the normal gland. The immunohistochemical distribution of keratin types between basal tumor cells of adenolymphoma and ductal basal cells of the normal salivary gland was compared.
Detection of the apoptosis-suppressing oncoprotein bcl-2 in salivary gland lymphoma.
The bcl-2 proto-oncogene encodes an inner mitochondrial membrane protein that blocks apoptosis and programmed cell death in human lymphoid tissue. In this study a monospecific anti-human bcl-2 antibody that is reactive in formalin-fixed tissues was used with an avidin-biotin complex immunoperoxidase method to evaluate 41 cases of lymphoproliferative disorders of the salivary gland. The study cases were 26 primary salivary gland lymphomas (including 21 B-cell lymphomas four T-cell lymphomas and one true histiocytic lymphoma) and 15 cases of myoepithelial sialadenitis. Bcl-2 expression is restricted to the mantle zone and interfollicular lymphocytes around reactive germinal centers of myoepithelial sialadenitis. Seventeen of the 21 B-cell lymphomas were positive for bcl-2, and were composed of mucosa-associated lymphoid tissue (MALT), centrocytic, centroblastic-centrocytic and centroblastic lymphomas. Noticeably, all 11 cases of MALT lymphoma were bcl-2 positive. In contrast, staining for bcl-2 was present in only one of four cases of T-cell lymphomas and was negative in one true histiocytic lymphoma. The expression of bcl-2 protein was also investigated in the ductal systems and epimyoepithelial islands of salivary glands from patients with malignant lymphoma and myoepithelial sialadenitis. While salivary ducts in eight of 15 cases of myoepithelial sialadenitis immunostained for bcl-2, epimyoepithelial islands showed bcl-2 expression in only five cases of myoepithelial sialadenitis. We found that ductal cells in the salivary gland from patients with primary non-Hodgkin's lymphomas expressed bcl-2 protein. It was of interest that epimyoepithelial islands in all cases of MALT lymphoma displayed bcl-2 expression whereas other subtypes of B-cell lymphoma, T-cell lymphoma and true histiocytic lymphoma were invariably negative. These results indicate that bcl-2 is expressed in a wide variety of non-Hodgkin's lymphomas, especially when all 11 cases of MALT lymphoma are bcl-2 positive. Epimyoepithelial islands in MALT lymphoma express this oncoprotein, and their ability to induce bcl-2 synthesis resulted in the prevention of apoptosis and prolonged cell survival. Furthermore, the expression of bcl-2 protein in the lymphoma cells may be responsible for the induction of bcl-2 expression in the adjacent epimyoepithelial islands through a lymphocyte chemical mediator.
Pleomorphic adenoma of the palate in a child: 9-year follow-up.
Pleomorphic adenoma (PA), the most common of the benign salivary gland tumors, is an extremely rare entity in children before the age of 14 years. Until now, only five cases arising in the palate have been reported in detail. A case of PA of the hard palate in a 10-year-old girl is presented. After a 9-year follow-up period, no recurrence was observed.