Ney Soares de Araújo

Carcinoma ex pleomorphic adenoma (CXPA): immunoprofile of the cells involved in carcinomatous progression

Aims : To characterize the cellular component in pleomorphic adenoma (PA) that undergoes malignant transformation in carcinoma ex pleomorphic adenoma (CXPA).

Characterization of the cellular component of polymorphous low-grade adenocarcinoma by immunohistochemistry and electron microscopy

In order to characterize the cellular component of the polymorphous low-grade adenocarcinoma (PLGA) of the salivary gland, a morphological and immunohistochemical study was carried out. Thirty cases of PLGA were studied by light microscopy and immunohistochemistry and five cases by transmission electron microscopy (TEM). The expression of cytokeratins (CKs) 7,8,10,13,14,18,19, vimentin and muscle-specific actin (MSA) was investigated through the streptavidin-biotin method. The majority of tumor cells stained for vimentin, CKs 8, 18 and 7. CK 14 was positive in most cells of the papillary and trabecular sub-types. Although the expression of CKs 8,18 and 14 varied among the tumors sub-types, a straight relationship between each histologic pattern and the CK expression could not be delineated. MSA was reactive in only three tumors while CKs 10 and 13 were not detected in any tumor studied. The absence of MSA and the expression of CKs 8,18 and 7, in most of the tumor cells, lead to the hypothesis that myoepithelial cells are not the major cellular component of the PLGA. TEM revealed cells exhibiting microvilli and variable amounts of secretory granules, some of them suggesting an excretory activity. The presence of CKs 8,18 and 7, added to the secretory granules, indicates that PLGA originates from cells located at the acinar-intercalated duct junction.

Actin versus vimentin in myoepithelial cells of salivary gland tumors: A comparative study

Vimentin versus actin expression was immunohistochemically studied in myoepithelial cells of 24 salivary gland tumors in which the participation of myoepithelial cells as a tumoral component has been postulated: two basal cell adenomas, seven pleomorphic adenomas, two myoepitheliomas, seven adenoid cystic carcinomas (two tubular, four cribriform, one solid), six polymorphous low-grade adenocarcinomas. Immunostaining was carried out in formalin-fixed tissue serial sections (3 microns) by the avidin-biotin method, using the antibody vimentin (Dako Corp., Carpenteria, Calif.) and the antibody HHF35 anti-muscle actin (Enzo Biochemical, N.Y.). Our results have confirmed positive staining for vimentin in all salivary tumors studied, although in some tumors it was only in focal areas. The staining for the HHF35 antibody to muscle actin was only consistently found in the adenoid cystic carcinomas of the tubular and cribriform patterns. This study suggests that actin is at least somewhat replaced by vimentin in neoplastic tumoral cells. Therefore vimentin can be used to define the participation and distribution of myoepithelial cells in these tumors.

Extranodal follicular dendritic cell sarcoma of the palate

Follicular dendritic cell tumors are uncommon and usually occur in lymph nodes. We report the case of a follicular dendritic cell tumor that occurred in the palate of a 14-year-old boy and manifested itself as a nodular mass. Histologically, the neoplasm consisted of spindle-shaped or oval-shaped cells with eosinophilic cytoplasms and nuclei with delicate, dispersed chromatin. The lesional cells were principally arranged in diffuse, fascicular patterns with vaguely whorled or storiform areas. Focal multinucleate tumor giant cells and lymphocytes were observed throughout the neoplasm. Immunohistochemically, tumor cells were positive for the follicular dendritic cell markers CD21, CD35, and CD23 and for S-100 protein, CD68, and muscle-specific actin. Tumor cells were negative for LCA, CD20, EMA, CK (AE1/AE3), HMB45, and CD34. Lymphocytes were positive for LCA and CD45RO. Although follicular dendritic cell sarcoma is a very uncommon tumor, it should be included in the differential diagnosis of tumors in this location.

Study of minor salivary gland mucoepidermoid carcinoma differentiation based on immunohistochemical expression of cytokeratins, vimentin and muscle-specific actin

The expression of cytokeratins (CKs) 7,8,10,13,14,18,19, vimentin and muscle-specific actin (MSA) was investigated in 17 mucoepidermoid carcinomas (MEC) by the streptavidin-biotin technique. The results revealed that CKs 7, 8 and 18 were positive for intermediate, luminal columnar and mucous cells. For epidermoid cells, the expression was heterogeneous and discrete. The reaction with CK19 was similar to that seen for the above CKs, except for the fact that mucous cells were negative. CK 14 was preferentially expressed in the intermediate cells localised in basal, parabasal and epidermoid cells. CK13 was localised in intermediate, epidermoid and luminal columnar cells. In stratified epithelium, CK13 was expressed in intermediate cells and negative in basal cells. These findings were more expressive in cystic areas of the tumours. CK10 was negative for all the cases studied. MSA was positive only in stromal elements, and only two cases of CME were heterogeneously positive for vimentin. The result obtained showed that the immunoprofile of MEC, for the studied antigens, is similar to that exhibited by the excretory duct of normal salivary glands.

Polymorphous low-grade adenocarcinoma and adenoid cystic carcinoma: distinct architectural composition revealed by collagen IV, laminin and their integrin ligands (α2β1 and α3β1)

Aims:

Immunohistochemical distinction of high-grade mucoepidermoid carcinoma and epidermoid carcinoma of the parotid region

The correct diagnosis of high-grade mucoepidermoid (MEC), which is composed of solid islands of intermediate and squamous cells, may be challenging, due to its similarity to other tumours, mainly with squamous cell carcinoma (SCC). The present report employed immunohistochemical technique against different cytokeratins (CKs), in order to differentiate these two entities. : Six high-grade MEC and six SCC of the parotid region, retrieved from the files of both Oral Pathology Department of the School of Dentistry of University of São Paulo and Pathology Department of A.C. Camargo Hospital, were submitted immunohistochemical technique against Cks 7,8, 10, 13, 14 and 19. : High-grade MEC was positive for Cks 7, 8, 13, 14 and 19. The cases of SCC showed strong positivity for CK14, and CK10 was present only in focal areas. Our results highlight the use of CKs (especially CK14) to differentiate high-grade MEC and SCC.

Healing of the displaced condylar process fracture: an experimental study

Healing of the displaced condylar process fracture was analysed by means of an experimental model using adults rats. Displaced fractures of the right condylar process were achieved under general anaesthesia. Histological data initially demonstrated neutrophilic exudation along the articular capsule and adjacent muscle fibres. One week later, devitalized bone areas at the fracture site, as well as proliferation of cartilaginous and osseous tissue were observed. Subsequently, exuberant callus formation and a decrease in the inflammatory process occurred. After 3 months, the condylar process presented characteristics of normality and was centralized into the temporal fossa, with interposition of the articular disc. These results indicate that experimentally induced, displaced condylar process fractures heal by callus formation with simultaneous repositioning of the condyle.

β-Catenin and E-Cadherin Expression in Salivary Gland Tumors

This study evaluated the expression of E-cadherin and β-catenin in salivary gland tumors. Twelve biopsy specimens from cases diagnosed as pleomorphic adenoma, 17 adenoid cystic carcinomas, 10 epithelial-myoepithelial carcinomas, and 4 polymorphous low-grade adenocarcinomas were immunohistochemically labeled for E-cadherin and β-catenin antibodies. Healthy salivary glands were used as controls. Membrane-associated E-cadherin and β-catenin expression was present in all the tumor types studied. E-cadherin and β-catenin showed a similar distribution; however, β-catenin labeling was weaker than that for E-cadherin. In the epithelial-myoepithelial carcinomas, myoepithelial cells exhibited diffuse nuclear staining, although occasional cells presented only focal labeling. Epithelial-myoepithelial carcinomas present changes in [.beta]-catenin expression but the other salivary tumors studied do not, which may reflect divergence in tumorigenesis of this extensive subset of salivary gland tumors.

Effect of N-CAM on in vitro invasion of human adenoid cystic carcinoma cells

Adenoid cystic carcinoma of salivary glands is characterised by aggressive behaviour, high rate of local recurrences, neurotropism and late metastasis. In a previous work we demonstrated that adenoid cystic carcinoma cultured cells (CAC2 cells) expressed N-CAM. It was suggested that this expression, modulated by extracellular matrix, would be correlated to cell movement. The aim of our study was to verify whether CAC2 cells presented invasion capacity. Moreover, we tested whether the neural adhesion molecule (N-CAM) would participate in this process. CAC2 cells were either previously treated, or not (control), with a monoclonal antibody against N-CAM. Invasion assays were carried out using a modified Boyden chamber (Transwell chamber). CAC2 cells (10(5)) were dispensed into Transwell upper chamber on the top of Matrigel coated filter. The cells that invaded the filters in the first 8 h were counted under light microscopy, yielding data for the invasion rates (%). Control CAC2 cells presented an invasion rate of 5.28+/-0.04%. The invasion rate raised to 6.53+/-0.2% when N-CAM was blocked with monoclonal antibody. N-CAM impaired the adenoid cystic carcinoma cell invasion in vitro. Therefore, we suggest an anti-invasive role for N-CAM in adenoid cystic carcinoma.