Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred and two cases of benign sweat gland tumors of the skin were studied for the presence of myoepithelial cells specifically identified by a monoclonal antibody to alpha-smooth muscle actin on paraffin-embedded tissues. The monoclonal antibody gave a positive result in 12 of 12 cases of cylindroma, 14 of 16 cases of spiradenoma, 2 of 2 cases of apocrine tubular adenoma (papillary eccrine adenoma), 5 of 5 cases of apocrine hidrocystoma, 5 of 5 cases of hidradenoma papilliferum, and in 10 of 10 cases of syringocystadenoma papilliferum. Rare myoepithelial cells were detected in only 1 of 10 cases of mixed tumor, apocrine type. There was no immunoreactivity for alpha-smooth muscle actin in eccrine hidrocystoma (2 cases), mixed tumor of eccrine type (2 cases), syringoma (7 cases), hidroacanthoma simplex (1 case), eccrine poroma (14 cases), clear cell hidradenoma (15 cases), and in 1 case of eccrine syringofibroadenoma. Our data support the concept that myoepithelial cells are seen in most sweat gland tumors considered to differentiate toward the secretory coil of the normal sweat gland. In contrast, myoepithelial cells are absent in tumors showing differentiation toward the excretory (ductal) component of the gland.
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PMID:Myoepithelial differentiation in benign sweat gland tumors. Demonstrated by a monoclonal antibody to alpha-smooth muscle actin. 133 Dec 11

We have evaluated by means of immunocytochemistry the distribution of various cytoskeletal and contractile proteins (cytokeratins, vimentin, desmin and alpha-smooth muscle actin) in 23 salivary or lacrimal gland primary tumours (15 pleomorphic adenomas and 8 carcinomas in pleomorphic adenoma), one third of which contained areas of normal gland. Normal epithelial luminal cells were stained by cytokeratin antibodies with a general specificity, while myoepithelial cells were selectively stained by a monoclonal antibody (SK2-27) reacting in immunoblots with cytokeratin polypeptides 14, 16 and 17, according to the classification of Moll et al. (1982) and by an antibody directed against alpha-smooth muscle actin (Skalli et al. 1986). In pleomorphic adenomas, both epithelial and myoepithelial cells displayed typical topographic distributions; moreover, myoepithelial cells showed two distinct cytoskeletal phenotypes. These findings could account in part for the heterogeneity of aspects observed in this tumour. In carcinomas, malignant cells were always positive to cytokeratin antibodies with general specificity and myoepithelial cells were absent as judged by anticytokeratin SK2-27 and anti-alpha-smooth muscle actin immunostainings. However, interestingly, there was in all cases a strong positivity for alpha-smooth muscle actin in stromal cells, similarly to what has previously been described for mammary carcinoma (Skalli et al. 1986). Our findings may be useful for the interpretation of the histogenesis of salivary and lacrimal tumour and stromal cells.
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PMID:Distribution of cytoskeletal and contractile proteins in normal and tumour bearing salivary and lacrimal glands. 283 Jul 13

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.
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PMID:[Immunohistological investigation of the histological origin and differentiation of pleomorphic adenoma of the parotid gland]. 769 Aug 50

A rapidly growing mandibular tumor occurred in a 17 month old female infant. Tumor outgrowth showing a periosteal reaction was radiographically seen on the lower surface (base) of the mandible. Under the biopsy diagnosis of osteosarcoma, high-dose chemotherapy with methotrexate was performed, resulting in little effect. The right hemimandibulectomy specimen disclosed intraosseous infiltrative growth of pleomorphic adenoma of salivary gland type, associated with chondroid stroma and reactive bone formation. The highly proliferative small-sized cells retained immunohistochemical features of myoepithelial cells, with positive reactivity of cytokeratin, vimentin, S-100 protein, alpha-smooth muscle actin, epithelial membrane antigen, CA15-3, type IV collagen, laminin and p53 protein. No heterotopia of the salivary gland was identified within the bone tissue. The tumor recurred 2 months later. Due to uncontrollable local growth, the patient died 8 months after operation. At autopsy, reactive ossification was closely associated with malignant myoepithelial proliferation. No distant metastasis was noted. This osteosarcoma-like tumor can be regarded as myoepithelial carcinoma in pleomorphic adenoma, originating from intramandibular heterotopic salivary gland tissue.
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PMID:Myoepithelial carcinoma in pleomorphic adenoma of salivary gland type, occurring in the mandible of an infant. 854 41

We studied the presence of myoepithelial cells (MCs) in the benign and malignant sweat gland adenomas by immunostaining with antibody to alpha-smooth muscle actin. We found peripheral arrangement of MCs in the neoplastic nests in cutaneous cylindromas (9), spiradenomas (13), syringoadenomas (7), and one case of adenoid cystic carcinoma. Dispersed MCs were identified in some cases of nodular hidradenoma (7/13) and malignant portion of spiradenocarcinoma (2/3). The remnants of the peripheral arrangement of MCs were retained in the benign part in cylindrocarcinoma and every case of spiradenocarcinoma, likewise in composed malignant adnexoma (malignisation within cylindroma/spiradenoma). We could not find MCs in papillary eccrine adenoma (2), poromas (7) and porocarcinomas (3), syringomas (6), chondroid syringomas (3), malignant nodular hidradenoma (1) and malignant portion of syringoadenoma (1). In one of three cases of eccrine hidradenocarcinoma focal myoepithelial differentiation could be identified at the periphery of the epithelial nests. These results confirm heterogeneity of the differentiation in sweat gland tumors, emphasizing the validity of division of those tumors into those with the differentiation towards secretory and ductal portion of the gland. The former group demonstrates the variability of arrangement of myoepithelial cells depending on the degree of dedifferentiation of the developing carcinoma. These cells may be replaced by outgrowing tumor, but may also accompany the neoplastic growth. Less significant is the presence of the MCs in the adenomas with ductal differentiation, which either in benign and malignant tumors may be lacking. The variability of MCs occurrence in cutaneous adenomas and carcinomas precludes its significance as a solitary factor in the differentiation between benign and malignant proliferations.
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PMID:Diagnostic significance of the myoepithelial cells in the benign and malignant sweat gland tumors. 870 71

A case of papillary eccrine adenoma on the right forearm of a 78-year-old Japanese woman is reported. The tumor was 1.3 cm in diameter, occupying the whole thickness of the dermis. Histologically, the tumor was composed of dilated tubules of various sizes with intraluminal papillary projections, and was surrounded by a fibrous stroma. An immunohistochemical study revealed that the proliferating tubules were composed of a single outermost layer of alpha-smooth muscle actin- and keratin 14-positive myoepithelial cells, and keratin 8-positive inner cells. This antigen expression pattern was comparable to that of the normal eccrine secretory coil, which indicates that the tumor differentiated toward the secretory coil of an eccrine sweat gland.
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PMID:Papillary eccrine adenoma: immunohistochemical study and literature review. 950 46

Predominant benign plasmacytoid myoepithelial cells in pleomorphic adenoma and malignant plasmacytoid myoepithelioma cells were investigated morphologically. The cells of both tumors were plasmacytoid in appearance and sheet-like. Immunohistochemically, they were positive for keratin, vimentin, and S-100 protein, and negative for alpha-smooth muscle actin. In the malignant cells, large nuclei with irregular nuclear membranes and distinct nucleoi and occasional intranuclear inclusions and nuclear grooves were seen. Ultrastructural findings showed that the benign cells were richer in intermediate filaments and had fewer mitochondria. The intranuclear inclusions and nuclear grooves of the malignant cells were caused by invagination of the irregular nuclear membranes. Taken in their entirety, the above light microscopical nuclear findings may be useful as an adjunct for distinguishing malignant from benign plasmacytoid neoplastic myoepithelial cells of the salivary gland.
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PMID:Malignant plasmacytoid myoepithelioma of the palate: histological observations compared to benign predominant plasmacytoid myoepithelial cells in pleomorphic adenoma of the palate. 961 85

The morphogenesis of salivary gland pleomorphic adenoma was examined in vitro using three-dimensional (3-D) collagen gel culture. Pleomorphic adenoma cells were isolated from three parotid gland tumours and cultured as monolayers, after which they were subcultured in floating-collagen gel sandwiches. Cells cultured in both conditions were immunohistochemically characterized and compared using antibodies against various proteins representative of each histological component of salivary glands. Monolayers had myoepithelial characteristics, being positive for vimentin and alpha-smooth muscle actin. In collagen gels, however, the cells assembled in epithelial nests, showing an architecture similar to that of pleomorphic adenoma. The nests were composed of duct-lining epithelial cells that were positive for epithelial markers, surrounded by myoepithelial cells. Collagen gel culture induces multidirectional differentiation of adenoma cells, suggesting that pleomorphic adenomas originate from stem or reserve cells.
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PMID:Reconstruction of pleomorphic adenoma of the salivary glands in three-dimensional collagen gel matrix culture. 1007 Dec 48

In order to examine stromal-epithelial interaction during the oncogenic progression of large bowel tumors, the association between pericryptal fibroblast sheath (PCFS) and expression of Ki-67 antigen was evaluated in 87 cases of colorectal adenoma and 95 cases of carcinoma with an adenoma component (CWA). For the immunohistochemistry, anti-alpha-smooth muscle actin antibody (alpha-SMA) and anti-Ki-67 antigen antibody (MIB-1) were used. In adenomas and adenoma components of CWA, the quantity of neoplastic glands with PCFS was reduced relative to the progression of histological atypia. Pericryptal fibroblast sheath was virtually absent from invasive carcinoma areas of CWA. Increased expression of Ki-67 correlated with the degree of histological atypia of adenomas. A significant reverse correlation was also seen between Ki-67 expression and PCFS-positive glands in adenoma components of CWA. These findings suggest that the prevalence of PCFS and Ki-67 expression are important indicators of colorectal neoplasia progression. The significant reduction of PCFS in colorectal epithelial neoplasms reflects progression in the adenoma-carcinoma sequence.
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PMID:Immunohistochemical analysis of pericryptal fibroblast sheath and proliferating epithelial cells in human colorectal adenomas and carcinomas with adenoma components. 1041 86

To investigate the development and progression of colorectal carcinoma, submucosal invasive carcinoma (SMC) with residual intramucosal neoplasm was studied histopathologically. Intramucosal neoplasm was confirmed by immunohistochemical staining against anti-alpha-smooth muscle actin antibody. Submucosal invasive carcinoma was classified into polypoid growth-type carcinoma (PGC) and non-polypoid growth-type carcinoma (NPGC), depending on the presence of intramucosal tumor proliferation. Tumors were > 15 mm in size in 78.2% of the PGC lesions studied, but the degree of submucosal invasion was minimal (invasion of the upper 500 microm of the submucosal layer) in 52.9% of the PGC lesions. Conversely, 64.4% of NPGC lesions were 15 mm in size and the degree of submucosal invasion was moderate or severe (involving the middle and deeper layer of the submucosa) for 72.9% of NPGC. In other words, lesions of NPGC were significantly smaller in size but showed deeper infiltration than PGC lesions. Furthermore, PGC was derived from intramucosal polypoid carcinoma (including carcinoma with adenoma) and was morphologically identical to polyp cancer as reported previously. However, NPGC was derived from the flat and/or depressed type of intramucosal carcinoma classified not as polyp type, but as the superficial type. Typical NPGC was, therefore, also of the superficial type. In addition, approximately 25% of PGC lesions were identified as having an adenoma-carcinoma sequence. There was no coexistence with adenoma in the NPGC lesions, suggesting de novo development. When the degree of histologic atypia in the two types of intramucosal carcinoma was compared, 74.7% of PGC lesions showed low-grade carcinoma, regardless of tumor size, while 62.7% of NPGC lesions showed high-grade carcinoma in the intramucosal lesion. Approximately 25% of carcinomas with low-grade atypia were positive for p53 (as were the high-grade lesions), but it was not expressed in the adenoma. Therefore, tumor development and the degree of invasion differed significantly between the two types of carcinoma.
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PMID:Histologic and immunohistochemical analysis of early submucosal invasive carcinoma of the colon and rectum. 1050 21


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