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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adhesion molecules such as CD44 play an important role in the metastatic cascade by mediating tumor cell interaction with the endothelium and the subendothelial matrix. As a so-called "lymphocyte homing receptor," CD44 is physiologically involved in migration of circulating lymphocytes to lymphatic tissue. In the present study, we investigated the expression of CD44v3 and v6 in 237 patients with stage IB, N0 cervical carcinoma by means of immunohistochemistry. These results were correlated with the GOG score and other prognostic variables. Median follow-up was 82.6 months (39-110 months). Thirty-nine patients recurred and 35 died from disease within the observation period. In univariate analysis, the GOG score, histologic subtype, and CD44v6 expression were statistically significant predictors for poor overall survival (OS). In multivariate (Cox regression) analysis, the GOG score (< 40 vs. 40-120, RR: 1.37 (95% CI: 1.10-1.71); 40-120 vs. > 120, RR: 2.23 (95% CI: 1.28-3.88); P = 0.004), histologic subtype (adenosquamous carcinomas) (RR: 4.56 (95% CI: 1.49-13.92), P = 0.007) and CD44v6 expression (RR: 2.42 (95% CI: 1.14-5.10), P = 0.021) were independent predictors for poor OS. The expression of CD44v3 did not correlate with prognosis. Furthermore we found a strong correlation between CD44v6 expression and lymphovascular space invasion (LVSI) (chi2 = 17.01, P = 0.0001). Tumor expansion into the loco-regional lymphatic system is the preferred way of tumor spread in cervical carcinoma. The strong correlation of CD44v6 with LVSI produces a significant degree of suspicion that cervical carcinoma cells expressing CD44v6 could, by mimicking lymphocytes, exploit their pathways.
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PMID:CD44v6 expression is an independent prognostic factor in node-negative FIGO stage IB cervical carcinoma. 1124 Jul 59

Integrins play an important role in tumour progression by influencing cellular responses and matrix-dependent adhesion. However, the regulation of matrix-dependent adhesion assembly in epithelial cells is poorly understood. We have investigated the integrin and signalling requirements of cell-matrix adhesion assembly in colon carcinoma cells after plating on fibronectin. Adhesion assembly in these, and in the adenoma cells from which they were derived, was largely dependent on alpha v beta 6 integrin and required phosphorylation of FAK on tyrosine-397. The rate of fibronectin-induced adhesion assembly and the expression of both alpha v beta 6 integrin and FAK were increased during the adenoma-to-carcinoma transition. The matrix-dependent adhesion assembly process, particularly the final stages of complex protrusion that is required for optimal cell spreading, required the activity of extracellular signal-regulated kinase (ERK). Furthermore, phosphorylated ERK was targeted to newly forming cell--matrix adhesions in the carcinoma cells but not the adenoma cells, and inhibition of FAK--tyrosine-397 phosphorylation or MEK suppressed the appearance of phosphorylated ERK at peripheral sites. In addition, inhibition of MEK--ERK activation blocked the formation of peripheral actin microspikes that were necessary for the protrusive phase of cell-matrix adhesion assembly. Thus, MEK--ERK--dependent peripheral actin re-organization is required for the full development of integrin-induced adhesions and this pathway is stimulated in an in vitro model of colon cancer progression.
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PMID:The protrusive phase and full development of integrin-dependent adhesions in colon epithelial cells require FAK- and ERK-mediated actin spike formation: deregulation in cancer cells. 1149 15

Prostate cancer metastasis to bone marrow involves initial adhesion of tumor cells to the bone marrow endothelium, followed by transmigration and proliferation within the marrow. Rapid, specific adhesion of highly metastatic prostate adenocarcinoma cells (PC3M-LN4) to bone marrow endothelial cell (BMEC) lines requires a pericellular hyaluronan (HA) matrix and correlates with dramatically up-regulated HA synthase (HAS) expression. Non-metastatic prostate tumor cells (LNCaP) do not assemble a HA matrix, adhere poorly to BMECs, and express normal levels of HAS. Preferential bone metastasis of prostate carcinoma cells may therefore be facilitated by tumor cell HA biosynthesis. In this report, HAS gene expression was manipulated to investigate the direct impact of prostate tumor cell HA production on adhesion to BMECs. PC3M-LN4 cells stably transfected with antisense HAS2 and HAS3 failed to form pericellular matrices. Adhesion of these transfectants to BMECs was significantly diminished, comparable to the low level exhibited by LNCaP cells. Upon transfection with full-length HAS2 or HAS3, the non-adherent LNCaP cells retained pericellular HA and adhered to BMECs. The results of this study are consistent with a model in which HA matrix formation, BMEC adhesion, and metastatic potential are mediated by HAS expression.
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PMID:Manipulation of hyaluronan synthase expression in prostate adenocarcinoma cells alters pericellular matrix retention and adhesion to bone marrow endothelial cells. 1179 Jul 79

Adhesion molecules are important in cell-cell and cell-basement membrane interactions. They are intimately involved in inflammatory reactions and a role in tumour progression has been postulated. E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) play a role in cell adhesion to the vascular endothelium, and may have a role in tumour cell dissemination. Soluble forms of these molecules have been described and this study was established to examine these adhesion molecules in patients with breast carcinoma. Serum was obtained from 92 patients with breast carcinoma and 31 age-matched patients with benign breast disease. All samples were obtained prior to surgery. Soluble levels of E-selectin, ICAM-1, and VCAM-1 were significantly elevated in patients with Stage 4 disease compared with controls. (E-selectin 88.6 (47.9) versus 51.4 (18.4) ng/ml; P<0.001: ICAM-1 447 (249) versus 244 (79) ng/ml; P<0.001: VCAM-1 779 (159) versus 552 (135) ng/ml; P<0.001 results expressed on mean (SEM) SD placed above this.). The prognostic value of the adhesion molecules was examined. In patients with Stage 2 disease, elevated VCAM-1 was predictive of decreased survival, even when corrected for T and N status. Adhesion molecules are elevated in patients with advanced disease and elevation in VCAM-1 has prognostic significance in patients with breast carcinoma.
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PMID:Soluble adhesion molecules (E-selectin, ICAM-1 and VCAM-1) in breast carcinoma. 1244 Dec 61

Adhesion between neighbouring epithelial cells is a crucial and tightly controlled process. In the gastrointestinal tract, the integrity of cell-cell contacts is essential for the regulation of electrolyte absorption and for the prevention of tumour metastasis. We recently showed that migration of the gastric epithelial cell line IMGE-5 is stimulated by the nonamidated form of the hormone gastrin(17). Here, we examine the effect on cell-cell adhesion of the prohormone progastrin, the concentration of which is increased in the plasma of patients with colorectal carcinoma. Progastrin induced the dissociation of both tight junction (TJ) and adherens junction (AJ) complexes in IMGE-5 cells. In progastrin-secreting DLD-1 human colorectal carcinoma cells, expression of an antisense gastrin construct restored membrane localisation of zonula occludens-1 (ZO-1), occludin, beta-catenin and E-cadherin. This restoration was reversed by treatment with exogenous progastrin. Endogenous or exogenous progastrin also increased the paracellular flux of mannitol, and induced cell migration of several gastrointestinal cell lines. In addition, progastrin enhanced Src tyrosine kinase activity and induced a spatial delocalisation of protein kinase C alpha. Using dominant-negative mutants and pharmacological inhibitors, we showed that the stimulation of Src kinase activity was essential for the regulation of TJs. By contrast, the dissociation of AJs involved phosphatidylinositol 3-kinase, partly through the formation of a complex with protein kinase C alpha. We conclude that separate pathways mediate the disruption of AJs and TJs by progastrin. Either pathway may contribute to the co-carcinogenic role of this prohormone in colorectal carcinoma.
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PMID:Adherens junctions and tight junctions are regulated via different pathways by progastrin in epithelial cells. 1261 62

Their adhesion to the intestinal mucosa is considered one of the main reasons for the beneficial health effects of specific lactic acid bacteria (LAB). However, the influence of disease on the mucosal adhesion is largely unknown. Adhesion of selected LAB to resected colonic tissue and mucus was determined in patients with three major intestinal diseases (i.e., diverticulitis, rectal carcinoma, and inflammatory bowel disease) and compared to healthy control tissue. All strains were observed to adhere better to immobilized mucus than to whole intestinal tissue. Two strains (Lactobacillus rhamnosus strain GG and L. reuteri) were found to exhibit disease-specific adhesion to intestinal tissue. All tested strains, with the exception of L. rhamnosus strain GG, displayed disease-specific adhesion to intestinal mucus. These results suggest that strains with optimal binding characteristics for a particular intestinal disease can be selected.
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PMID:Disease-dependent adhesion of lactic acid bacteria to the human intestinal mucosa. 1285 98

OBJECTIVE:The present study was to investigate the expression of CD44s and CD44v6 in human salivary adenoid cystic carcinoma (ACC) and to discuss the relationship between the expression of the proteins and the biological characteristic of ACC.METHODS:Formalin fixed,paraffin embedded sections in 10 cases of normal salivary glands and 50 cases of human salivary ACC were examined using immunostaining for CD44s and CD44v6.RESULTS:(1)Positive signals of CD44s and CD44v6 were detected in all the specimens of normal salivary glands.Positive signals of CD44s and CD44v6 were detected in 29(58%) and 35(70%) of the 50 cases of ACC.(2)The expression of CD44s and CD44v6 in the solid pattern of ACC was significantly less than that in the cribriform and tubular pattern of ACC(P<0.05).(3)Positive CD44s staining was detected in 3(13.6%) of the 22 ACC primary sites which had a local recurrence after operation.CONCLUSION:(1)Adhesion molecules including CD44s and CD44v6 may contribute to maintain the normal structures in salivary gland tissues.(2)T he down-regulation or loss of CD44s expression was contributed to the recurrence of human salivary ACC and CD44s could be regarded as one of the factors to evaluate the prognosis of ACC patients.
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PMID:[The expression of CD44s and CD44v6 in human salivary adenoid cystic carcinoma ] 1504 49

ObJECTIVE:Observation the affection of aspirin to adhesion of highly metastatic salivary adenoid cystic carcinoma(ACC-M) cell induced by platelet.METHODS:Adhesive ratios of ACC-M cell induced by platelet with or without aspirin were measured.RESULTS:After the addition of platelet rich plasma(PRP),adhesive ratio of ACC-M cell increased significantly (P<0.01). The treatment with aspirin after addition of PRP led to a nonsignificant increase of adhesive ratio (P>0.05).The reduction of adhesive ratio by aspirin was found dosage independent within concentration range of 0.01-0.25g/L of aspirin. CONCLUSION:Adhesion of ACC-M cell was raised by added platelet.Addition of aspirin,platelet induced adhesion of ACC-M cell was inhibited significantly.
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PMID:[The in vitro comparison of platelet induced ACC-M cell adhesion with and without Aspirin] 1504 67

Adhesion molecules play an important role in tumor metastasis. E-selectin can support adhesion of colon cancer cells through the recognition of specific carbohydrate ligands. High levels of soluble E-selectin (sE-selectin) had been reported in melanoma and some epithelial tumors, especially in colorectal carcinoma. The concentrations of the sE-selectin were investigated in serum samples of 64 patients (32 men and 32 women) with colorectal cancer and 16 healthy subjects. Median age was 57 (range 20-75). Nineteen patients were staged as Dukes D, 9 of whom had liver metastasis. Serum levels of sE-selectin were determined by ELISA. In the study group, sE-selectin concentrations (mean+/-SE, ng/ml) were not significantly elevated, compared with the control group (41.09+/-4.57 in the control group and 43.80+/-1.88 in patients, p>0.05). Mean sE-selectin levels were 42.27+/-1.85 in non-metastatic and 47.42+/-4.57 in metastatic patients (p>0.05). Serum concentrations of sE-selectin were significantly elevated in patients with colorectal cancer metastatic to liver (59.07+/-7.52) in comparison to other patients without liver metastasis (p=0.013). There were no significant correlations between sE-selectin levels and other parameters such as age of patients, stage of disease, histopathological differentiation or localization of primary tumor. Elevated sE-selectin levels were confirmed as correlating with poor overall survival. In conclusion, sE-selectin concentrations may not be used as a predictive marker of metastasis in colorectal carcinoma, but high levels of sE-selectin may support diagnosis of liver metastasis.
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PMID:Serum levels of soluble E-selectin in colorectal cancer. 1525 58

Integrin-mediated adhesion of epithelial cells to extracellular matrix (ECM) proteins induces prolonged tyrosine phosphorylation and partial activation of epidermal growth factor receptor (EGFR) in an integrin-dependent and EGFR ligand-independent manner. Integrin-mediated activation of EGFR in epithelial cells is required for multiple signal transduction events previously shown to be induced by cell adhesion to matrix proteins, including tyrosine phosphorylation of Shc, Cbl, and phospholipase Cgamma, and activation of the Ras/Erk and phosphatidylinositol 3'-kinase/Akt signaling pathways. In contrast, activation of focal adhesion kinase, Src, and protein kinase C, adhesion to matrix proteins, cell spreading, migration, and actin cytoskeletal rearrangements are induced independently of EGFR kinase activity. The ability of integrins to induce the activation of EGFR and its subsequent regulation of Erk and Akt activation permitted adhesion-dependent induction of cyclin D1 and p21, Rb phosphorylation, and activation of cdk4 in epithelial cells in the absence of exogenous growth factors. Adhesion of epithelial cells to the ECM failed to efficiently induce degradation of p27, to induce cdk2 activity, or to induce Myc and cyclin A synthesis; subsequently, cells did not progress into S phase. Treatment of ECM-adherent cells with EGF, or overexpression of EGFR or Myc, resulted in restoration of late-G(1) cell cycle events and progression into S phase. These results indicate that partial activation of EGFR by integrin receptors plays an important role in mediating events triggered by epithelial cell attachment to ECM; EGFR is necessary for activation of multiple integrin-induced signaling enzymes and sufficient for early events in G(1) cell cycle progression. Furthermore, these findings suggest that EGFR or Myc overexpression may provoke ligand-independent proliferation in matrix-attached cells in vivo and could contribute to carcinoma development.
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PMID:Epidermal growth factor receptor-dependent regulation of integrin-mediated signaling and cell cycle entry in epithelial cells. 1536 78


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