Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Xanthogranulomatous cholecystitis (XGC) is a focal or diffuse destructive inflammatory process of the gall bladder, characterized macroscopically by yellowish tumour-like masses in the wall of the gall bladder. Microscopically, it is characterized in the early stages by a large number of foamy histiocytes and acute inflammatory cells. Later stages demonstrate increasing fibrosis. The gall bladder from 20 of 352 consecutive patients subjected to cholecystectomy showed XGC. Gall stones were found in the gall bladder of all 20 patients and in the ductus choledochus in 3 cases. Perforation of the gall bladder was observed at operation in six cases; in one case there was also a fistula to the colon. A perivesical abscess was found in five other cases. Adhesions to the surrounding structures were seen in a total of 16 cases. Pathogenetically, XGC is probably due to an interplay between obstruction of the gall flow, infection with subsequent inflammation, and leakage of gall fluid to the tissue, where histiocytes accumulate and phagocytize the bile pigment, haemosiderin and cholesterol, resulting in the formation of xanthoma cells. The correct diagnosis of XGC is important for several reasons, first and foremost due to the high frequency of complications, but not least because the condition may give rise peroperatively to the suspicion of malignancy. The new laparoscopic method for cholecystectomies further stresses the necessity of correct preoperative diagnosis of complicating disease.
 ...
PMID:Xanthogranulomatous cholecystitis. A clinicopathological study of 20 cases and review of the literature. 828 95

Adhesion under hydrodynamic flow is a step in many complicated physiological processes such as the neutrophil-mediated inflammatory response and cancer cell metastasis. We use a combination of computer simulation and experiment to explore how a population of cells interacts with a ligand-coated substrate under shear flow. To simulate the binding of a single cell to a surface, we use a microvilli-hard sphere model in which receptor-ligand bonds are treated as springs, and the net motion of the cell is determined from a force balance involving hydrodynamic, bonding, and colloidal forces. We show that the adhesive phenotype of a cell depends strongly on the fractional spring slippage of receptor-ligand bonds, which relates the extension of a bond to its rate of breakage; a lower spring slippage indicates bonds can withstand a great deal of extension without a significant increase in the breakage rate, and hence leads to more strongly adherent cells. We construct the behavior of a population of cells by simulating many cells using this algorithm. We show that a homogeneous population of cells with identical numbers of receptors, modeled with parameters suitable to recreate neutrophil rolling, will display a distribution of translational velocities. In addition, we calculate the average velocity for a heterogeneous population of cells which has a Gaussian distribution in receptor number. As the standard deviation of this distribution increases, the average observed velocity for the population increases. Although the homogeneous and heterogeneous populations have the same average number of receptors (10(5)) per cell, there is a significant difference in their average velocity when the standard deviation of receptor number in the heterogeneous population is as little as 25% of the average receptor number. We also present experimental evidence that not all cells exhibit the slow rolling characteristic of neutrophil-endothelial interaction, but rather appear to exist in a "binary" state in which cells are either adherent or noninteracting. We have developed an experimental model system for studying adhesion under hydrodynamic flow, using the rat basophilic leukemia (RBL) derivatized polyacrylamide gels in a flow chamber. Cells are injected into a portion of the flow chamber in which the substrate is not coated with antigen, and allowed to flow over the antigen-coated portion of the gel. We have measured the spatial distribution of cell binding for a population of cells at different flow rates, and have shown that cell binding decreases as shear rate increases.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Statistics of cell adhesion under hydrodynamic flow: simulation and experiment. 831 63

Tumor cell interaction with endothelial cells is a crucial step leading to organ-selective metastasis. Adhesion of murine B16 amelanotic melanoma cells (B16a) to murine microvascular endothelial cells (CD3) was enhanced, in a dose- and time-dependent manner, by pretreating CD3 cells with 12(S)-hydroperoxyeicosatetraenoic acid [i.e., 12(S)-HETE], a 12-lipoxygenase metabolite of arachidonic acid. The metabolic precursor of 12(S)-HETE, 12-HPETE (12-hydroperoxyeicosatetraenoic acid) also enhanced B16a cell adhesion to CD3 monolayers, whereas other lipoxygenase products, i.e., 5(S), 11(S), and 15(S)-HETEs were ineffective. 12(S)-HETE-enhanced tumor cell adhesion was blocked by treating endothelial cells with antibodies against the alpha v beta 3 complex or against individual subunits but not with antibodies against alpha 5 beta 1. In contrast, neither of these two integrins appeared to be involved in tumor cell adhesion to unstimulated endothelium. Flow cytometric analysis, immunofluorescent labeling, and image analysis indicated that 12(S)-HETE induced a time- and dose-dependent increase in the surface expression of alpha v beta 3 but not alpha 5 beta 1 on CD3 cells. The increased surface expression of alpha v beta 3 on endothelial cells did not result from an increased transcription or translation of alpha v beta 3 message as confirmed by quantitative reverse transcription-polymerase chain reaction, Northern blotting, and quantitative Western blotting. Instead, subcellular fractionation studies revealed an increased translocation of alpha v beta 3 integrins from the cytosolic pool to the membrane fractions. Pretreatment of endothelial cells with several cytoskeleton-disrupting agents (i.e., cycloheximide or acrylamide to disrupt intermediate filament vimentin, cytochalasin D to disrupt microfilaments, colchicine or Nocodazole to disrupt microtubules) abolished the 12(S)-HETE-enhanced alpha v beta 3 surface expression as well as tumor cell adhesion to endothelial cells. Also, pretreatment of CD3 cells with protein kinase C inhibitor calphostin C, but not with protein kinase A inhibitor H8, blocked 12(S)-HETE-enhanced alpha v beta 3 surface expression and tumor cell adhesion. Collectively, these results suggest that eicosanoid 12(S)-HETE modulates tumor cell interaction with endothelium via protein kinase C- and cytoskeleton-dependent up-regulation of the surface expression of alpha v beta 3 integrin.
Cancer Res 1994 Feb 15
PMID:Activation of microvascular endothelium by eicosanoid 12(S)-hydroxyeicosatetraenoic acid leads to enhanced tumor cell adhesion via up-regulation of surface expression of alpha v beta 3 integrin: a posttranscriptional, protein kinase C- and cytoskeleton-dependent process. 831 70

Epithelial cancer of the ovary spreads by implantation of tumor cells onto the mesothelial lining of the peritoneal cavity. We have developed an in vitro binding assay using confluent monolayers of normal peritoneal mesothelial cells in order to assess the role of known adhesion proteins in this process. Cells from normal ovarian surface epithelium and the ovarian cancer cell lines CAOV-3 and SKOV-3 exhibited significant adhesion to mesothelium in vitro (range 33-56% specific binding). Although these cells expressed several adhesion molecules, including CD44 and integrins such as alpha 4 beta 1, alpha 5 beta 1, and alpha v beta 3, only anti-CD44 antibody was capable of inhibiting mesothelial binding (range 42-44% inhibition). Adhesion molecule expression was also determined for fresh ovarian specimens, with CD44 being expressed in 2 of 2 cases of normal ovarian epithelium, 15 of 16 (94%) cases of tissue-derived tumor (from primary sites or peritoneal implants), and only 2 of 8 (25%) cases of free-floating tumor cells from ascites. Three of three CD44-positive cases derived from peritoneal implants exhibited significant mesothelial binding which was partly blocked by anti-CD44 antibody, whereas 2 of 2 CD44-negative cases derived from ascites showed minimal binding. CD44-mediated binding of ovarian cancer cells was determined to be due to recognition of mesothelium-associated hyaluronate, suggesting that the CD44H isoform was involved in this process. Immunoprecipitation of the CD44 species expressed by ovarian cancer cells revealed 2 major bands at 85-90 and 180 kDa, consistent with the known molecular masses of CD44H. These results suggest that CD44H may be an important mediator of ovarian cancer cell implantation and that decreased CD44H expression may be associated with release of cells into the peritoneal space during ascites formation. It is possible that strategies to interfere with CD44H function may result in decreased intraabdominal spread of this highly lethal neoplasm.
Cancer Res 1993 Aug 15
PMID:Binding of ovarian cancer cells to peritoneal mesothelium in vitro is partly mediated by CD44H. 833 95

Adhesion molecules are thought to play a vital role in the induction and maintenance of tissue differentiation and their loss or down-regulation has been implicated in the neoplastic process. Recent studies have shown that the morphoregulatory activities are a consequence of interactive processes between several cell adhesion molecules rather than the function of a single molecule. Therefore, we have investigated a panel of adhesion molecules including members of the integrin, cadherin and immunoglobin superfamily in colorectal cancer. Twenty-eight consecutive colorectal adenocarcinomas were stained using an avidin-biotin indirect immunoperoxidase technique. Our results showed a consistent loss of the alpha 2 and beta 1 integrin subunits (21/28 = 75% and 22/28 = 78.6% respectively) and a decrease in expression of E-cadherin in 5/5 poorly differentiated adenocarcinomas. Carcinoembryonic antigen expression was preserved but with basolateral accentuation seen in tumours. There was no statistical correlation with Dukes' stage. These results provide further evidence that in colorectal cancer there is a widespread deregulated expression of cell-cell and cell-matrix adhesion molecules. Changes in the expression and function of adhesion molecules which regulate growth and differentiation may play a role in the behaviour of colorectal cancer.
Br J Cancer 1993 Sep
PMID:Loss of cell-cell and cell-matrix adhesion molecules in colorectal cancer. 835 41

The use of percutaneous transcatheter hepatic arterial chemotherapy and embolization in the treatment of primary liver cancer has become increasingly popular in recent years. The authors employed this method, using a combination of cisplatin, mitomycin C, 5-fluorouracil, and ethiodized oil (Lipiodol) or absorbable gelatin sponge in 30 patients with huge liver cancers (diameter range, 5.6-12.0 cm) as a preliminary treatment before liver resection. Significant tumor regression occurred after this treatment, converting these tumors into resectable lesions that were excised successfully later. Before surgery, chemoembolization was done once every 4-6 weeks. The patients underwent 1-5 treatment sessions (mean, 2.9) and then waited 1-4 months (mean, 2.4 months) before undergoing surgery. Alpha-fetoprotein levels decreased to normal in seven patients. The tumor diameters were reduced by 31.6 +/- 15.2% (2.3 +/- 1.2 cm) and the percent tumor necrotic area ranged from 40-100%. Adhesions of the tumor to the diaphragm and thickening of the hepatoduodenal ligament and gallbladder wall were the primary operative findings, but they did not significantly complicate the surgery. There was one postoperative death from acute pulmonary embolism. The 1-year, 2-year, and 3-year survival rates were 88.89%, 77.03%, and 77.03%, respectively. Although these patients still are being followed to assess their long-term survival, this treatment appears promising for patients with advanced huge liver cancers who hitherto have been denied surgery on grounds of unresectability.
Cancer 1993 Jan 01
PMID:Experience with liver resection after hepatic arterial chemoembolization for hepatocellular carcinoma. 838 Jan 23

We compared integrin-mediated adhesion to extracellular matrix (ECM) components of cultured human melanocytes and 6 human melanoma cell lines with different metastatic capacities in nude mice. Cultured melanocytes and most melanoma cell lines adhered strongly to fibronectin (FN), whereas only highly metastatic cell lines adhered to laminin (LM), collagen type I (COI) and type IV (COIV). Adhesion to LM and CO could be blocked by anti-alpha 6 and anti-alpha 2 monoclonal antibodies (MAbs) respectively. This observation is consistent with the finding that expression of LM receptor alpha 6 beta 1 and LM/CO receptor alpha 2 beta 1 was low on melanocytes and non- or poorly metastatic cell lines, whereas these integrins were strongly expressed on highly metastatic cell lines. In addition, immunoprecipitation from [35S]-methionine-labeled cells demonstrated increased synthesis of alpha 6, alpha 2 and beta 1 in highly metastatic cell lines and immunohistochemistry showed expression of alpha 6 beta 1 and alpha 2 beta 1 only in xenograft lesions from highly metastatic cell lines. Furthermore, the observation that adhesion of melanocytes and non- or poorly metastatic cell lines could be stimulated with anti beta 1 MAbs demonstrates that these receptors, on these cells, are expressed in an inactive state. Our results suggest that alpha 2 beta 1 and alpha 6 beta 1 play a role in human melanoma metastasis in nude mice and demonstrate that interactions of these integrins with their ligands can be regulated at the level of surface expression and activation state of the receptor.
Int J Cancer 1993 May 08
PMID:Regulation of integrin-mediated adhesion to laminin and collagen in human melanocytes and in non-metastatic and highly metastatic human melanoma cells. 838 65

It is now clear that adhesive interactions play a critical role in the process of metastatic tumor dissemination. Adhesion molecules act as both positive and negative modulators of the metastatic process. Molecules such as E-cadherin that promote homotypic tumor cell adhesion function to maintain intercellular contacts that confine cells to the primary tumor site and are negatively correlated with metastatic potential. Because tumor cells are rapidly eliminated from the circulation, those cells that can quickly arrest in the vasculature at a secondary site and pass through the vessel wall into the surrounding tissue will have a selective advantage toward establishing new metastatic colonies. The first step in this process is specific adhesion to venular endothelial cells in selected organs, a process mediated by tumor cell surface molecules such as Sialyl LewisX or the VLA-4 (alpha 4 beta 1) integrin that mediate binding to endothelial adhesion molecules such as the E-selectin or the vascular cell adhesion molecule, VCAM-1. Site-specific endothelial determinants such as the lung endothelial cell adhesion molecule, LuECAM, may additionally specify particular sites for preferential adhesion and subsequent site-specific metastasis of particular tumor types. After adherence to endothelial cells and subsequent endothelial retraction, metastatic tumor cells must adhere to elements of the subendothelial basement membrane such as laminin and types IV and V collagen, interactions frequently mediated by members of the beta 1 and beta 4 integrin families. Finally, metastatic tumor cell adhesion to connective tissue elements such as fibronectin, type I collagen and hyaluronan, mediated by molecules such as the beta 1 integrins and by the CD44 cell surface adhesion molecule, are required for movement of tumor cells into the subendothelial stroma and subsequent growth at these new sites. Thus, metastatic potential can be influenced both positively and negatively by a variety of cell surface adhesive molecules that act both independently and in concert to direct tumor cells to particular tissues, allowing them to arrest in those tissues, migrate across the vessel wall and grow at the secondary site. In the current review, I discuss the nature of the adhesion molecules that have been implicated in the metastatic process, emphasizing those molecules that have been shown to correlate with metastasis in clinical human tumors or that have been shown to influence metastatic potential in in vivo experimental assays.
Semin Cancer Biol 1993 Aug
PMID:Adhesion molecules in tumor metastasis. 840 Jan 43

Adhesion molecules are essential components of immunitary response and inflammation. Adhesion molecules could be classified as integrins, selectins, immunoglobulins superfamily and carbohydrates. The role of adhesion molecules in inflammation, immunity cancer, acute respiratory diseases, transplantation and his possible relevance in therapy are reviewed and discussed.
 ...
PMID:Adhesion molecules in immunity and inflammation. 847 Nov 39

Galectin-3 is a laminin binding protein which expression is altered in a variety of human carcinomas including colon, breast and endometrium. In these tumors, we consistently observed a down regulation of galectin-3 expression related to increased aggressiveness. Galectin-3 belongs to a family of galactose-binding lectins and binds laminin through its numerous poly-N-acetyllactosamine chains. To date, the exact role of galectin-3 in the complex interactions between cancer cells and laminin has not been clearly defined. Adhesion of melanoma cells to laminin is a critical event during tumor invasion and metastasis. In this study, we explore the possibility that galectin-3 could modulate attachment of two human melanoma cell lines to laminin. A2058 and A375 melanoma cell expressed galectin-3 on their surface as demonstrated by immunofluorescence, and attached to laminin in an in vitro assay. We demonstrate that neither recombinant galectin-3 nor an affinity purified antigalectin-3 antiserum altered adhesion of A2058 or A375 melanoma cells to laminin. Our data strongly suggest that galectin-3 is not a key element in adhesion of the melanoma cells to laminin. These results are not surprising in light of the observation that galectin-3 expression is down regulated in cancer and that increased adhesion to laminin is a constant feature of invasive cancer cells.
 ...
PMID:Galectin-3, a laminin binding protein, fails to modulate adhesion of human melanoma cells to laminin. 855 98


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>