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)

Cadherin is an Ca2+ dependent adhesion molecules, which contribute to cell-cell adhesion and maintenance of tissue structures. Its decrease or functional abnormality plays an important vole in cancer invasion and metastasis. We investigate the expression of E- cadherin in thyroid neoplasms (papillary cancer, follicular cancer, medullary cancer anaplastic cancer and follicular adenoma) and normal thyroid. The decrease of E-cadherin expression in thyroid cancer correlates with its malignancy and metastatic potentiality.
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PMID:[Expression of E-cadherin in thyroid neoplastic tissues and its correlation with malignant and metastatic potential]. 762 98

The homotypic homophilic cell-cell adhesion molecule E-cadherin is crucial in the organization and maintenance of most epithelia. The expression of E-cadherin was studied immunohistochemically in various human colorectal tumours. Therefore we stained 1 tubular adenoma with low grade dysplasia, 18 adenocarcinomas with different histologic degrees of differentiation and invasion, and 1 metastasis using a modified peroxidase-anti-peroxidase technique. In the adenoma as well as in all well differentiated adenocarcinomas we found E-cadherin immunopositivity at the cell membrane of almost all cancer cells. The immunopositivity of E-cadherin was clearly weaker and sometimes even absent in isolated neoplastic cells and glands of less differentiated adenocarcinomas. The moderately differentiated adenocarcinomas showed an intermediate staining pattern. These findings are in line with experimental evidence that downregulation of E-cadherin favours invasion, eventually leading to metastasis.
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PMID:Immunohistochemical analysis of E-cadherin expression in human colorectal tumours. 830 30

Reduced expression of E-cadherin has been associated with loss of differentiation and/or increased invasiveness and metastatic ability in several types of neoplasms. Rare studies on thyroid tumors have shown minimal or absent expression in undifferentiated carcinomas and a variable degree of immunoreactivity/mRNA expression in follicular and papillary carcinomas. We studied immunohistochemically 2 follicular adenomas, 8 follicular carcinomas, 18 papillary carcinomas and 3 poorly differentiated carcinomas to evaluate E-cadherin expression. In 7 papillary carcinomas, lymph node metastases were also studied. The E-cadherin gene was analysed in 27 tumors by PCR/SSCP followed, whenever appropriate, by DNA sequencing. LOH at the E-cadherin locus was assessed in 16 tumors. Reduced and heterogeneous expression of E-cadherin was found in primary and metastatic papillary carcinomas, whereas follicular carcinomas showed moderate to strong homogeneous immunoreactivity, and poorly differentiated carcinomas showed no or very faint immunoreactivity. The only case harbouring a (missense type) mutation of the E-cadherin gene was a papillary carcinoma exhibiting immunoreactivity in the primary tumor as well as in metastasis. LOH was found in a follicular adenoma and in a poorly differentiated carcinoma without evidence of mutation in the remaining allele. Our results show that irreversible alterations (allele loss or mutation) of the E-cadherin gene are infrequent in thyroid tumors. The reduced and heterogeneous expression of E-cadherin in thyroid carcinomas, particularly of the papillary histotype, appears to reflect transcriptional regulation or post-transcriptional modulation rather than structural abnormalities.
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PMID:E-cadherin gene alterations are rare events in thyroid tumors. 898 87

Little is known about the the signalling pathways driving the adenoma-to-carcinoma sequence in human colonic epithelial cells. Accumulation and activation of the src tyrosine kinase in colon cancer suggest a potential role of this oncogene in this early progression. Therefore, we introduced either activated src (m-src), polyoma-MT alone or combined with normal c-src in the adenoma PC/AA/C1 cell line (PC) to define the function and phenotypic transformations induced by these oncogenes in familial adenomatous polyposis (FAP) colonic epithelial cells. Functional expression of these oncoproteins induced the adenoma-to-carcinoma conversion, overexpression of the hepatocyte growth factor (HGF) receptor Met, but failed to confer invasiveness in vivo and in vitro, or to produce alterations in cell proliferation and differentiation. In contrast, PC-msrc cells became susceptible to the HGF-induced invasion of collagen gels and exhibited sustained activation of the pp60src tyrosine kinase and Tyr phosphorylation of the 120-kDa E-cadherin, which was further increased by HGF Transcripts of HGF were clearly identified by reverse transcription-polymerase chain reaction (RT-PCR) and Southern blot in the parental and transformed PC cells, suggesting an autocrine mechanism. Taken together, the data indicate that: (1) experimental activation of src and PyMT pathways directly induces tumorigenicity and Met upregulation in a colon adenoma cell line; (2) HGF-activated Met and src cooperate in inducing invasion; (3) in view of the molecular associations between catenins and cadherin or the tumour-suppressor gene product APC, the cell adhesion molecule E-cadherin may constitute a downstream effector of src and Met.
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PMID:Progression of familial adenomatous polyposis (FAP) colonic cells after transfer of the src or polyoma middle T oncogenes: cooperation between src and HGF/Met in invasion. 901 33

Development of malignant tumours is in part characterized by the ability of a tumour cell to overcome cell-cell adhesion and to invade surrounding tissue. E-cadherin is the main adhesion molecule of epithelia, and it has been implicated in carcinogenesis because it is frequently lost in human epithelial cancers. Re-establishing the functional cadherin complex in tumour cell lines results in a reversion from an invasive to a benign epithelial phenotype. However, it remained unresolved whether the loss of E-cadherin-mediated cell adhesion was a cause or a consequence of tumour progression in vivo. Here we report that the loss of E-cadherin expression coincides with the transition from well differentiated adenoma to invasive carcinoma in a transgenic mouse model of pancreatic beta-cell carcinogenesis (Rip1Tag2). Intercrossing Rip1Tag2 mice with transgenic mice that maintain E-cadherin expression in beta-tumour cells results in arrest of tumour development at the adenoma stage, whereas expression of a dominant-negative form of E-cadherin induces early invasion and metastasis. The results demonstrate that loss of E-cadherin-mediated cell adhesion is one rate-limiting step in the progression from adenoma to carcinoma.
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PMID:A causal role for E-cadherin in the transition from adenoma to carcinoma. 951 65

CD56/N-CAM antigen, 140 kDa isoform of neural cell adhesion molecule (N-CAM) has been previously traced by some of us in follicular epithelium of human thyroid by immunohistochemistry. The reaction product was cell membrane bound, being stronger in hyperactive thyroid as compared to colloid goiter. In the current study, CD56 was searched in other endocrine glands and their tumors including parathyroids, adrenal cortex and parafollicular C cells of the thyroid (TT cell line). The antigen was also examined in the tissue extracts of endocrine and nonendocrine organs by dot blot immunoassay and anti CD56 monoclonal antibody. Besides, some other cell adhesion molecules (CAMs) were looked for in the tissues and cells tested. It has been found that CD56 is expressed in all zones of adrenal cortex, albeit in various intensity. The reaction was cell membrane bound in cortical hyperplasia and adenoma but cytoplasmic in the carcinoma of adrenal cortex. Other endocrine tissues and cells tested were devoid of CD56. Presence of CD56 antigen could be confirmed by dot blot assay with 3M KCl and NP40 extracts of both, thyroid and adrenal glands. Apart from CD56 some other CAMs could be traced in thyroid cell membranes including CD44, VLA-3 integrin and E-cadherin, what was not the case in the adrenal cortex. In parathyroids and parathyroid adenoma, diffuse immunostaining of E-cadherin and irregular, focal expression of CD44 was observed. These results show, apart from CD56, abundance of other CAMs in the thyroid gland and their relative scarcity in other endocrine tissues tested.
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PMID:Expression of CD56/N-CAM antigen and some other adhesion molecules in various human endocrine glands. 977 95

E-cadherin is a member of the cadherin family that plays a major role in epithelial integrity and tumorigenesis. Catenins are a group of cytoplasmic proteins that regulate the intracellular anchorage of cadherin and are required for the linkage between cadherin and the actin cytoskeleton. Loss of E-cadherin contributes to the pathogenesis in tumor invasion and gives a poor prognosis. In order to investigate the adhesion property of intercellular junctions in thyroid tumors, expression of alpha-,beta, and gamma-catenin should also be studied. A correlation between these molecular markers and malignancy would be useful as a preoperative diagnostic test for thyroid neoplasms. The expression of E-cadherin, alpha-, beta-, and gamma-catenin were studied in normal and neoplastic thyroid tissue by immunofluorescence microscopy and Western blot analysis. In the normal thyroid and in nodular goiter, and follicular adenoma, staining for E-cadherin, alpha-, beta-, and gamma-catenin was seen mainly at the lateral surface of epithelial cells in the follicle and the presence of these molecules was confirmed by Western blot analysis. Follicular carcinoma tissue stained positive for E-cadherin and alpha-catenin, but the results of beta- and gamma-catenin immunostaining were highly variable, with beta-catenin being absent in most follicular carcinomas (8/10) and gamma-catenin being absent in some follicular carcinomas (3/10). These results suggest that E-cadherin expression was not reduced during the pathogenesis of differentiated thyroid malignancies. Impairment of the cadherin-catenin complex at the cell junction may contribute to the malignant progression of differentiated thyroid neoplastic tissue.
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PMID:Expression of the cadherin-catenin complex in well-differentiated human thyroid neoplastic tissue. 1059 58

Colorectal carcinoma is a major cause of death throughout the Western world. It is increasingly recognized that any reduction in mortality must be achieved through the detection and removal of early and precancerous lesions. The primary attention for such a preventive strategy has been the polypoid adenoma and surveillance studies have shown a significant reduction in the incidence of carcinoma through systematic polypectomy of suspicious lesions. A potential problem with such a program, however, is raised by reports from Japan that some carcinomas seem to arise without a precursor polypoid adenoma, that is de novo. Although the histopathologic findings in such reports seem to clearly support this idea, this concept is not widely accepted in the Western world. We undertook a series of immunohistochemical (p53, bcl-2, Mib-1, E-cadherin, CD44, Stromelysin-3), and microsatellite analysis studies (on 17p (p53), 18q (DCC), 5q (APC), 8p, 2p and 1p), on groups of de novo and ex adenoma carcinomas in order to see if differences between the two groups of lesions exist. The results of these studies demonstrate that de novo carcinomas share several phenotypic and genotypic features with ex adenoma carcinoma (similar CD44 in the carcinomas, similar rates of LOH at APC and DCC loci), but have significantly higher rates of LOH at 17p, p53 over-expression and ST-3 expression indicating that tumor progression in de novo carcinoma is accelerated. These findings should help clarify the concept of de novo carcinoma and contribute to wider recognition of this important clinicopathologic entity.
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PMID:[Are there differences between ex adenoma and de novo colorectal carcinomas?]. 1071 4

E-cadherin is a cell surface molecule that mediates cell-cell adhesion in normal epithelium. Disabled or aberrant E-cadherin expression increases cell motility and promotes the transition of well-differentiated adenoma to invasive carcinoma. To evaluate whether E-cadherin could serve as a biomarker of squamous cell differentiation, we analyzed its expression by immunohistochemistry in formalin-fixed, paraffin-embedded tissue sections of 7 head and neck cancer patients, 19 lung cancer patients, 73 esophageal cancer patients, 19 skin cancer patients, and 18 cervical cancer patients. E-cadherin was expressed at very high levels (93%-100%) in adjacent or distant normal squamous epithelia. Likewise, most (75-100%) well-differentiated squamous cell carcinomas (SCCs) also expressed E-cadherin. In contrast, poorly differentiated SCCs expressed less than 40% of E-cadherin. Furthermore, immunohistochemical analysis showed that the differentiation-inducing agent, all-trans retinoic acid, can up-regulate E-cadherin expression in esophageal SCC cells in vitro. Our data demonstrated that E-cadherin expression is associated with SCC differentiation and that may serve as a squamous cell differentiation marker.
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PMID:Expression of E-cadherin is associated with squamous differentiation in squamous cell carcinomas. 1092 48

To investigate whether expression of E-cadherin correlates with polarised tissue organisation, grade or tumour type in salivary neoplasms, frozen sections from 30 salivary gland neoplasms were stained immunohistochemically for E-cadherin using the antibody HECD-1 and compared to the staining patterns in five samples of normal salivary gland. Lesions with areas of lack of staining were restained at two higher antibody concentrations. Normal salivary gland stained strongly around the periphery of acinar and ductal cells. Neoplasms mostly stained strongly regardless of neoplasm type. Reproducible loss of expression was found only in epithelial cells showing stromal or plasmacytoid (hyaline) differentiation in pleomorphic adenoma. Low- and high- grade mucoepidermoid carcinomas, adenocarcinoma NOS and carcinoma ex pleomorphic adenoma showed focal loss of expression but this was not related to tissue architecture, differentiation or invasiveness. We conclude that the relationship seen between E-cadherin expression and cell polarity/glandular organisation in breast and colon does not appear to exist for salivary gland neoplasms in which the diversity of architectural patterns precludes detection of any simple relationship. E-cadherin expression seems unlikely to be a useful marker for diagnosis or prognosis in salivary neoplasia in general.
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PMID:Expression of E-cadherin, cellular differentiation and polarity in epithelial salivary neoplasms. 1103 44


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