Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04626 (erbB-2)
 5,251 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acquired cystic disease of the kidney (ACDK) reveals abnormal epithelial cell growth which suggests a cotinuum of cyst, adenoma and renal cell carcinoma (RCC). In the present study, we examined potential role of vimentin and growth factors for cyst growth and proliferation in 20 cases with ACDK by immunoperoxidase staining method. 1281 cysts with single-layered epithelia and 89 cysts with multi-layered epithelia (atypical cyst) were studied. Intermediated filament, vimentin was positive in staining in 41.6% of cysts with single-layered epithelia, in 73.1% of cyst with multi-layered epithelia and in 100% of adenomas and RCCs. Vimentin expression, therefore, may be considered as an indication of cellular differentiation among proliferating tubular or intracystic cells. In order to evaluate the growth and/or proliferative capabilities of cyst epithelia, epidermal growth factor (EGF), epidermal growth factor receptor (EGFR) and c-erb B2 gene product were determined in cyst epithelia, adenoma and adenocarcinoma. EGF showed positive staining in 49.1% of cyst with single-layered epithelia, in 68.4% of cyst with multi-layered epithelia, in 2 of 3 adenomas and in 5 of 8 RCCs. EGFR expression was observed in 61.7% of cyst with single-layered epithelia, in 94.7% of cyst with multi-layered epithelia, in 100% of adenomas and RCCs. Co-expression of EGF and EGFR was observed in 40.3% of cyst with single-layered epithelia and in 67.1% of cyst with multi-layered epithelia. C-erb B2 gene product was positive in 9.7% of cyst with single-layered epithelia, in 100% of cyst with multi-layered epithelia and in 3 of 7 RCCs. These findings indicate that the expression of vimentin and overexpression of these growth factors and receptors appear to be one of the mechanisms operating in potentiating the abnormal growth of cyst epithelia, including potential for oncogenesis of RCC.
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PMID:[Immunohistochemical study in acquired cystic disease of the kidney--expression of vimentin, epidermal growth factor, epidermal growth factor receptor and c-erb B2 gene product]. 810 22

The goat was chosen as the model system for investigating mammary gland development in the ruminant. Histological and immunocytochemical staining of goat mammary tissue at key stages of development was performed to characterize the histogenesis of the ruminant mammary gland. The mammary gland of the virgin adult goat consisted of a ductal system terminating in lobules of ductules. Lobuloalveolar development of ductules occurred during pregnancy and lactation which was followed by the regression of secretory alveoli at involution. The ductal system was separated from the surrounding stroma by a basement membrane which was defined by antisera raised against laminin and Type IV collagen. Vimentin, smooth-muscle actin and myosin monoclonal antisera as well as antisera to cytokeratin 18 and multiple cytokeratins stained a layer of myoepithelial cells which surround the ductal epithelium. Staining of luminal epithelial cells by monoclonal antibodies to cytokeratins was dependent on their location along the ductal system, from intense staining in ducts to variable staining in ductules. The staining of epithelial cells by monoclonals to cytokeratins also varied according to the developmental status of the goat, being maximal in virgin and involuting glands, lowest at lactation and intermediate during gestation. In addition, cuboidal cells, situated perpendicular to myoepithelial cells and adjacent to alveolar cells in secretory alveoli, were also stained by cytokeratin monoclonal antibodies and antisera to the receptor protein, erbB-2, in similar fashion to luminal epithelial cells. These results demonstrate that caprine mammary epithelial cell differentiation along the alveolar pathway is associated with the loss of certain types of cytokeratins and that undifferentiated and secretory alveolar epithelial cells are present within lactating goat mammary alveoli.
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PMID:Identification of cell types in the developing goat mammary gland. 1046 24

It was hypothesized that four histopathological types or subtypes of breast carcinoma were undifferentiated types characterized by bidirectional differentiation toward both luminal epithelial and myoepithelial cells and had characteristic molecular changes: invasive ductal carcinoma (IDC) with a large central acellular zone, atypical medullary carcinoma (a subgroup in Grade 3 solid-tubular carcinoma), matrix-producing carcinoma, and spindle-cell carcinoma (or carcinoma with spindle-cell metaplasia). In 32 cases of the undifferentiated type and 37 cases of the relatively differentiated types, we immunohistochemically examined the expressions of myoepithelial markers and KIT, epidermal growth factor receptor (EGFR), and c-erbB-2 oncoproteins. Vimentin, S-100, and alpha-smooth muscle actin were positive in 28 (88%), 22 (69%), and 15 (47%) of the undifferentiated types, but were positive in seven (19%), one (3%), and one (3%) of relatively differentiated types (P < 0.0001). KIT and EGFR overexpressions were detected more frequently in the undifferentiated types (34 and 88%, respectively) than in relatively differentiated types (3 and 3%, respectively) (P < 0.0001, for both). In 11 (85%) of 13 cases with KIT overexpression, EGFR overexpression concurred. c-erbB-2 overexpression was almost equally detected in both the undifferentiated and relatively differentiated types, and did not correlate with KIT or EGFR overexpression. Phosphotyrosine was detected in 16 (67%) of 24 cases with KIT, EGFR, and/or c-erbB-2 overexpression but only in six (18%) of 34 cases without KIT, EGFR, or c-erbB-2 overexpression (P = 0.0002). The undifferentiated-type breast carcinomas appeared to show mammary epithelial stem cell-like features, and they could be identified by KIT and/or EGFR overexpressions.
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PMID:Frequent KIT and epidermal growth factor receptor overexpressions in undifferentiated-type breast carcinomas with 'stem-cell-like' features. 1595 55