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

To identify adhesion molecules involved in the formation of liver metastases, we prepared monoclonal antibodies against rat liver plasma membranes, that inhibited the adhesion of mouse metastatic TA3 mammary carcinoma cells to rat hepatocytes in vitro. Two such antibodies (designated OPAR-1 and OPAR-2) were obtained, that inhibited by over 70%. As assessed with gel electrophoresis and immunoblotting, these antibodies bound predominantly to plasma membrane proteins with molecular weights of 125,000 and 100,000. Using immunoelectron microscopy, the OPAR antigen was found to be abundantly present on the sinusoidal surface of hepatocytes, and in addition on contiguous hepatocyte surfaces and Kupffer cells, but was absent from sinusoidal endothelial cells. The tissue distribution and molecular weight indicate that the OPAR antigen is different from other hepatic adhesion molecules. Adhesion of MB6A lymphosarcoma cells was not inhibited by OPAR antibodies, indicating that these cells adhere to hepatocytes via a different surface molecule.
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PMID:Hepatocyte surface molecule involved in the adhesion of TA3 mammary carcinoma cells to rat hepatocyte cultures. 401 53

Mechanisms of adhesion between tumor cells and hepatocytes, which are likely to play a role in liver metastasis formation, were studied in vitro. TA3 mammary carcinoma and MB6A lymphosarcoma cells were added to rat hepatocytes that had been cultured for 24 hours. Adhesion was quantified by counting adherent cells seen in sections of pelleted, Epon-embedded culture fragments. Adhesion of TA3, but not of MB6A cells, was inhibited by antibodies prepared from an antiserum raised against sinusoidal face-enriched liver plasma membranes. Detergent-solubilized liver components, affinity purified on immobilized inhibitory antibodies, neutralized inhibition, whereas a subfraction separated from this material with the use of immobilized noninhibitory antiliver antibodies had no neutralizing activity. Adhesion of MB6A but not of TA3 cells was inhibited by the calcium ionophore A23187 and the local anesthetic procaine. The calmodulin inhibitor trifluoperazine inhibited adhesion of MB6A cells more strongly than that of TA3 cells. Finally, adhesion of TA3 cells was dependent on external calcium, whereas in the case of MB6A cells calcium could be replaced by magnesium. These observations suggested that adhesion of the two tumor cell types to hepatocytes involved distinct hepatocyte surface molecules and required distinct biochemical machinery.
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PMID:Adhesion of tumor cells to hepatocytes: different mechanisms for mammary carcinoma compared with lymphosarcoma cells. 643 81

An overview is presented of our studies on the interaction between blood-borne tumor cells and the tissues where metastases are formed, in particular the liver. Using blocking antibodies and tumor cell mutants, we have identified the adhesion molecules involved, which so far are all integrins. Strikingly, tumor cell lines that are quite similar, and invade in a comparable fashion, use distinct integrins. Lymphomas that invade the liver massively and diffusely use LFA-1 or fibronectin receptors to adhere to hepatocytes. We have obtained evidence that LFA-1 is activated during the interaction by factors that act through G-protein-coupled receptors, and preliminary results suggest that the same may be true for the fibronectin receptors. Whereas TA3/Ha murine mammary carcinoma cells adhere to hepatocytes via alpha 6 beta 4, TA3/St variant cells of the same tumor bind via the fibronectin receptor alpha 5 beta 1. Adhesion of the TA3/Ha cells appears to be impaired by the mucin epiglycanin that is abundantly present on the surface of these cells.
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PMID:The role of integrins and integrin activation in liver metastasis. 765 36