Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:B0FTZ7 (catenin)
 18,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are three macroscopic types of hepatic bile duct carcinoma, such as papillary (P-), nodular (N-) and diffuse (D-) type. Immunohistochemical studies demonstrated that P-type expressed cadherin and catenin higher than N- and D-types. The expressions of both cadherin and catenin were found stronger in pap and tub1 than tub2. The nuclear area of cancer cell, correlated with both labeling index of Ki-67 and aberrant accumulation of p53, was significantly larger in the subserosal layer than in the mucosal layer. These may explain the differences in the biological behavior between P- and N, D-types. P-type grows within the mucosal layer, while N- and d-type are more invasive, developing into the subserosal layer. Our clinical data also demonstrates the poor prognosis of N-, D-type of hepatic bile duct carcinoma. On these basis of the biological malignancy of N, D-type, it is critical to remain the surgical margin free from cancer cells to cure this type of hepatic bile duct carcinoma.
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PMID:[Mode of spreading and biological behavior in bile duct carcinoma]. 921 11

Bronchioloalveolar carcinoma (BAC) has features distinct from those of conventional pulmonary adenocarcinoma (CPA) in terms of its characteristic growth pattern along alveolar walls and intrapulmonary metastasis via the aerogenous route. We speculated, therefore, that BAC might differ from CPA in its capacity for cell-to-cell or cell-to-basement membrane adhesion. E-cadherin (E-CD), one of the most important elements of epithelial integrity molecules, is related to tumor metastasis in various organs. Differences of E-CD and associated catenin expressions between BAC and CPA, however, have not been elucidated. We examined the expression of E-CD and alpha-, beta- and gamma-catenin immunohistochemically in 18 BACs (9 mucinous, 7 nonmucinous, and 2 sclerosing) in comparison with CPAs, all of which were well-differentiated adenocarcinomas. In addition, we analyzed the correlation between the expression of these cell adhesion molecules and the presence of intrapulmonary metastasis, histologic subtypes, and cell proliferation activity. Clinicopathologically, we observed intrapulmonary metastases in 4 of the 18 BACs and none of the CPAs. In 14 of the 18 BACs, more than one-half of the tumor cells expressed E-CD, and the E-CD expression level was significantly higher in the BACs than in the CPAs. In addition, all of the BACs exhibited preserved membranous staining for E-CD, whereas in 5 of the 14 CPAs, the expression pattern was disorganized cytoplasmic staining; the difference was statistically significant. The Ki-67 labeling index was significantly lower in the BACs than in the CPAs. There were no appreciable differences in E-CD expression among the BAC subtypes. E-CD expression was significantly lower in the BACs with intrapulmonary metastasis than in the BACs without intrapulmonary metastasis. These findings indicated to us that BAC was distinct from CPA in terms of proliferation activity and expression of certain adhesion molecules and that E-CD downregulation was associated with a tendency toward intrapulmonary metastasis.
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PMID:Expression of E-cadherin, alpha-catenin, beta-catenin, and gamma-catenin in bronchioloalveolar carcinoma and conventional pulmonary adenocarcinoma: an immunohistochemical study. 983 Nov 99

E-cadherin/catenin (alpha-, beta-, and gamma-) complex plays a critical role in the control of epithelial differentiation. The aim of this study was to examine the immunoreactivity of E-cadherin and alpha-, beta-, and gamma-catenins in premalignant and malignant non-melanocytic skin tumours (NMST) and to correlate their expression with the grade of tumour differentiation, as assessed by the established histopathological criteria and by the Ki-67 index. Benign NMSTs were also studied. To investigate any possible influence of immunosuppression in the expression of E-cadherin and catenins, the study compared tumours obtained from renal transplant recipients (RTRs) and immunocompetent patients. Immunoperoxidase staining of E-cadherin and alpha-, beta-, and gamma-catenins was performed in 42 squamous cell carcinomas (SCCs) (26 from RTRs and 16 from non-RTRs), 30 lesions of Bowen's disease (11 from RTRs and 19 from non-RTRs), 11 atypical squamoproliferative lesions from RTRs, 19 actinic keratoses (9 from RTRs and 10 from non-RTRs), and 20 viral warts from RTRs. The findings of this study were as follows. Firstly, the probability of abnormal expression of E-cadherin and alpha-, beta-, and gamma-catenins increased from benign to premalignant and malignant NMSTs (p<0.001 for all). Secondly, there was agreement in abnormal expression between most of the molecules measured in malignant and premalignant NMSTs (p<0.05). Thirdly, in SCC, abnormal expression of E-cadherin and catenins was more frequent in lesions with a high (>40%) Ki-67 index than in those with a low Ki-67 index (<40%) (p=0.003). However, only the abnormal expression of gamma-catenin increased with the grade of SCC differentiation (p=0.008). Fourthly, abnormal expression of gamma-catenin predicted a high proliferation index (Ki-67 index 40%) in NMSTs (p<0.01, OR=6.19). Finally, there was no difference in the abnormal expression of E-cadherin and catenins between NMSTs from immunosuppressed and immunocompetent patients. Thus, abnormal expression of the E-cadherin/catenin complex was quite common in SCC and Bowen's disease and also in a proportion of intraepithelial dysplastic lesions, such as atypical squamoproliferative lesions and actinic keratosis, suggesting that these changes may be early indicators of the neoplastic process. Abnormal expression of gamma-catenin was the sole predictor of high proliferation in NMST and was also correlated with the tumour grade, suggesting a possible important role for gamma-catenin in tumourigenesis.
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PMID:Abnormal immunoreactivity of the E-cadherin/catenin (alpha-, beta-, and gamma-) complex in premalignant and malignant non-melanocytic skin tumours. 1179 66

Neuroendocrine tumors (NETs) of the gastrointestinal tract comprise a heterogeneous group of neoplasms arising from the diffuse neuroendocrine system. These tumors strongly differ from each other on the basis of different pathogenetic, clinical, functional, histological, and prognostic patterns. Previous studies have shown that abnormal and reduced expression of the E-cadherin/catenin complex in several human cancers is associated with tumor dedifferentiation, advanced clinical stages, and poor survival rate. We assessed correlations between the expression of E-cadherin and catenins, Ki-67, and the following clinicopathological factors: age, embryological site of origin, size, histological growth pattern, the depth of penetration into the intestinal wall, and the presence of metastasis. In this study, reduction of membranous E-cadherin expression to a variable degree was detected in more than two-thirds (42 of 51) of gastrointestinal NETs (19 foregut, 8 midgut, and 24 hindgut) belonging to the complete neuroendocrine neoplastic spectrum [18 well-differentiated NETs, 22 well-differentiated neuroendocrine carcinomas (NECs), and 11 poorly differentiated NECs]. The reduction of E-cadherin expression was concomitant with the reduction of alpha-catenin (44 of 51) and beta-catenin (35 of 51) expression. Our immunohistochemical analysis demonstrated significant differences of percentage of membranous positive cells of E-cadherin, alpha-catenin, or beta-catenin between normal tissues and well-differentiated NETs (P=0.0038, P=0.004, and P=0.0329, respectively), well-differentiated NECs (P<0.001, P<0.001, and P<0.001, respectively) and poorly differentiated NECs (P=0.0002, P<0.0002, and P=0.0002, respectively). Among the gastrointestinal NETs, there were significantly more positive cells of E-cadherin, alpha-catenin, or beta-catenin in well-differentiated NETs than well-differentiated NECs (P=0.0006, P=0.0065, and P=0.0001, respectively) or poorly differentiated NECs (P=0.0053, P=0.0041, and P<0.001, respectively). MIB-1 labeling index generally showed a low proliferative activity in well-differentiated NETs (0.49+/-0.37) and well-differentiated NECs (0.662+/-0.66). A high proliferation rate was observed in poorly differentiated NECs (41.518+/-16.59). MIB-1 labeling index was significantly higher in poorly differentiated NECs than well-differentiated NETs and well-differentiated NECs (P<0.0001 and P<0.0001, respectively). E-cadherin, alpha-catenin, and beta-catenin expression were correlated significantly with transmural tumor invasion (P<0.0001, P=0.0001, and P<0.0001, respectively) and with size (P=0.0013, P=0.0001, and P<0.0001, respectively). These results indicate that the alteration in the E-cadherin/catenin expression may be involved in the growth and progression of gastrointestinal NETs.
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PMID:Alterations of E-cadherin, alpha-catenin and beta-catenin expression in neuroendocrine tumors of the gastrointestinal tract. 1196 44

B -Catenin is closely associated with carcinoma invasion/metastasis and poor survival. Recent studies have demonstrated that abnormal expression of B -catenin, especially its nuclear accumulation, also plays an important role in wingless/Wnt signaling pathway. In this study, we evaluated immunohistochemically the nuclear localization of B -catenin in a total of 93 human-endocrine-related tumors including 1 medullary carcinoma (thyroid gland), 12 parathyroid tumors, 22 carcinoid tumors (digestive tract and liver), 7 islet cell tumors, 26 adrenocortical tumors, 13 neuroblastoma (adrenal gland), and 12 pheochromocytoma (adrenal gland), and also studied genetic alterations of the B -catenin gene. Nuclear accumulation of B -catenin was frequently detected in 8 of 22 (36%) carcinoid tumors and 2 of 7 (29%) islet cell tumors. No genetic alteration in exon 3 of the B -catenin gene encoding serine/threonine rich domain, which was phosphorylated by GSK-3 B, was detected in any groups of the endocrine tumors. However, nuclear accumulation of B -catenin in carcinoid tumors was significantly correlated with the proliferative marker Ki-67 (MIB-1) labeling index (p <0.001). Our findings suggest that nuclear transfer and accumulation of the B -catenin may contribute in the tumorigenesis of carcinoid tumor as an oncoprotein.
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PMID:Nuclear Accumulation of B-Catenin in Human Endocrine Tumors: Association with Ki-67 (MIB-1) Proliferative Activity. 1211 96

Goblet cell carcinoid (GCC) of the appendix is a rare entity, of which both the histogenesis and biologic behavior remain controversial, and prognostic tools and therapeutic strategies for this unusual tumor have yet to be defined. The aim of this study was to analyze expression of E-cadherin and b-catenin in GCCs of the appendix with long-term follow-up data as related to the expression of Ki-67 proliferation marker to provide a rationale for treatment guidelines. We analyzed the expression of E-cadherin, b-catenin, and Ki-67 in 11 GCCs of the appendix and control groups of typical carcinoids of the large intestine (n = 29), well to moderately differentiated adenocarcinomas of the colon (n = 10), poorly differentiated adenocarcinomas of the colon (n = 12), and normal appendiceal tissues (n = 10). There was no significant difference between the GCCs and normal appendiceal tissues regarding the expression of E-cadherin or b-catenin (p = 0.297 and 0.103, respectively). The percentage of positive GCC cells ranged between 0.52 and 10.35% (4.27 +/- 0.80), and only one case had a score >10%. Metastatic tumor spread and death were found in high MIB-1 labeling index (LI) cases of GCC (>3%). Our findings suggest that the behavior of the majority of GCCs might be indolent and different from adenocarcinomas because of the preserved expression of E-cadherin and b-catenin and relatively low MIB-1 LI. However, some of these tumors act aggressively and MIB-1 LI might be a good parameter to determine the therapeutic procedure.
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PMID:Expression of E-cadherin, b-catenin, and Ki-67 in goblet cell carcinoids of the appendix: an immunohistochemical study with clinical correlation. 1211 50

Cadherins are cell-surface glycoproteins that mediate Ca2+-dependent, homophilic cell-cell adhesion. The classical cadherins, E- and N-cadherins, connect to beta-catenin, the lining protein. There appears to be a relationship between their dysfunction and tumor invasion and metastasis. The aim of our study was to examine the possibility of a relationship between alterations in the E- and N-cadherin and catenin expression and malignancy in astrocytomas. Forty-five astrocytomas (18 glioblastomas, 16 anaplastic astrocytomas, and 11 diffuse astrocytomas) were collected and stained immunohistochemically for cadherins and beta-catenin. None of the astrocytomas were immunoreactive for E-cadherin. N-cadherin and beta-catenin were present at cell-cell borders in 61% of glioblastomas and 31% of anaplastic astrocytomas. The incidence of immunoreactivity for N-cadherin and beta-catenin increased significantly with the histological grade of astrocytomas (p = 0.001, by Kruskal-Wallis test). Moreover, in anaplastic astrocytomas and glioblastomas, the Ki-67 labeling indices in both N-cadherin-positive and beta-catenin-positive cases were higher than that in negative cases (p = 0.05 and 0.03, respectively, by Fisher's exact test). These results suggest that the expression of N-cadherin or beta-catenin may be related to the biological behavior of astrocytomas.
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PMID:Relationship between the expression of E-, N-cadherins and beta-catenin and tumor grade in astrocytomas. 1212 81

Cadherins are cell-surface glycoproteins that mediate Ca2+-dependent, homophilic cell-cell adhesion. The classical cadherins, E- and N-cadherins, bind to beta-catenin, the lining protein. Dysfunctional expression of these factors seems to be related to tumor invasion and metastasis. This study examined the relationship between changes in E- and N-cadherins, and catenin expression, and biological behavior in medulloblastomas and atypical teratoid/rhabdoid tumors. Specimens of 13 medulloblastomas and two atypical teratoma/rhabdoid tumors were collected and stained immunohistochemically to detect E- and N-cadherins, and beta-catenin. None of the medulloblastomas were immunoreactive for E-cadherin, but both atypical teratoma/rhabdoid tumors were immunoreactive for E-cadherin at the cell-cell borders where epithelial differentiation occurred. In contrast, N-cadherin and beta-catenin were present at the cell-cell borders in 12 of the 13 medulloblastomas and both atypical teratoma/rhabdoid tumors. Nuclear beta-catenin staining was not present in the medulloblastomas or atypical teratoma/rhabdoid tumors. There was no significant difference in the Ki-67 staining index between patients with medulloblastomas showing high and low immunoreactivity for N-cadherin and beta-catenin. Moreover, immunoreactivity for N-cadherin and beta-catenin increased with dissemination in the medulloblastomas. Low immunoreactivity in medulloblastomas tended to be associated with a better prognosis. These results suggest that expression of E-cadherin is useful for the differential diagnosis of atypical teratoma/rhabdoid tumor and medulloblastoma, and the expression of N-cadherin or beta-catenin may be related to the biological behavior of medulloblastomas.
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PMID:E, N-cadherins and beta-catenin expression in medulloblastoma and atypical teratoid/rhabdoid tumor. 1550 47

Female adnexal tumor of probable Wolffian origin (FATWO) is a rare entity which is believed to originate from mesonephric (Wolffian) remnants on the basis of its location where the remnants are abundant. Its behavior is usually indolent, although some cases can recur or metastasize. The authors present the clinicopathological features of two cases of FATWO arising in the broad ligament, and focus on the expression of adhesion molecules and proliferative marker. Mesonephric duct remnants are also examined in an attempt to elucidate the histogenesis of FATWOs. The two FATWOs were well-circumscribed solid masses arising in the leaves of the broad ligament and histological examination revealed a mixture of cysts and tubules imparting a sieve-like pattern and mucin-negative eosinophilic secretion within these tubules. Immunohistochemically, the tumors showed the expression of cytokeratin 7 and 20, high-molecular-weight cytokeratin, and calretinin, which closely resembled that of the mesonephric duct remnants. Regarding CK 20, CD 10, EMA, S-100 protein, and vimentin their expression was in part not identical with previous studies. E-cadherin, alpha and beta-catenin were strongly expressed along the cell membrane of the tumor cells. The Ki-67 labeling index of FATWO was 0% and 3.2% in each case. The preservation of the E-cadherin-catenin complex and low Ki-67 labeling index could explain the indolent behavior and low malignant potential of this tumor.
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PMID:Expression of adhesion molecules and Ki-67 in female adnexal tumor of probable Wolffian origin (FATWO): report of two cases and review of the literature. 1551 Dec 77

Prolactinoma is the most common pituitary tumour in adults. Macroprolactinomas, particularly in men, may occasionally exhibit a very aggressive clinical course as evidenced by progressive growth, invasion through bone into the sphenoid sinus, cavernous sinus, suprasellar region or the nasopharynx. Some may even progress to pituitary carcinoma with craniospinal or systemic metastases. Aggressive tumours have low cure rates despite appropriate medical and surgical treatment. The mechanisms underlying this aggressive biological behaviour have not yet been fully clarified. Recent immunohistochemical, molecular and genetic studies have provided some insight in this respect. Invasive prolactinomas may be associated with a high Ki-67/MIB-1 labelling index indicating increased cell proliferation, although this is not a universal finding. The AA polymorphism in the cyclin adenine (A)/guanine (G) gene is more frequently detected in invasive prolactinomas. Increased expression of the polysialylated neural cell adhesion molecule (NCAM) and reduced expression of the E-cadherin/catenin complex implies a contribution of altered cell-to-cell adhesion and cellular migration. Extracellular matrix components (ECM), matrix metalloproteinases (MMPs) and their inhibitors play important roles in the context of angiogenesis and invasion. The induction of fibroblast growth factor and vascular endothelial growth factor via oestrogen-induced overexpression of novel genes (PTTG, hst and Edpm5) enhance cell growth, proliferation and angiogenesis contributing to invasiveness in prolactinomas. Although mutations in proto-oncogenes like Ras are uncommon, loss of tumour suppressor genes at loci 11q13, 13q12-14, 10q and 1p seem to be associated with invasiveness. Of the described mechanisms, only reduced E-cadherin/catenin expression and overexpression of hst gene seem to be relatively specific markers for prolactinoma invasiveness compared with other pituitary adenomas. Further research is needed to clarify the molecular mechanisms behind the aggressive course of some prolactinomas to predict those with a potentially poor clinical outcome, and to devise treatments that will eventually enable the cure of these challenging tumours.
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PMID:What are the markers of aggressiveness in prolactinomas? Changes in cell biology, extracellular matrix components, angiogenesis and genetics. 1728 3


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