Hepatocyte surface molecule involved in the adhesion of TA3 mammary carcinoma cells to rat hepatocyte cultures.

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.

Adhesion of tumor cells to hepatocytes: different mechanisms for mammary carcinoma compared with lymphosarcoma cells.

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.

Interactions between lymphoid tumor cells and isolated liver endothelial cells.

Interactions were studied between highly metastatic murine MB6A lymphosarcoma cells and rat liver endothelial cells that had been isolated by collagenase perfusion and purified by unit gravity sedimentation. Experiments were performed on the day of isolation. MB6A cells were observed to adhere to the endothelial cells.

Infiltration of lymphosarcoma cells into hepatocyte cultures: inhibition by univalent antibodies against liver plasma membranes and lymphosarcoma cells.

The number of murine MB6A lymphosarcoma cells that infiltrated rat hepatocyte cultures was found to be diminished after treatment of the lymphosarcoma cells with univalent antibodies raised against these tumour cells (anti-MB6A Fab), and also after treatment of the hepatocyte cultures with univalent antibodies directed against rat liver plasma membranes (anti-LPM Fab). The inhibition of infiltration by anti-MB6A Fab and an anti-LPM Fab raised against sinusoidal face-enriched membranes could be entirely attributed to their interference with adhesion of MB6A cells to the exposed surface of the hepatocytes, because infiltration of the adherent cells was not inhibited. Anti-LPM Fab raised against contiguous face-containing LPM, on the other hand, inhibited the adhesion to the exposed surface and the subsequent infiltration of adherent cells.

Infiltration of tumour cells into cultures of isolated hepatocytes.

MB 6A lymphosarcoma and TA3 mammary carcinoma cells have previously been shown to infiltrate from liver blood vessels, where they had been arrested, into the liver parenchyma. The same tumour cells were previously added to cultures of isolated hepatocytes, 24 h after their isolation. Both tumour cell types adhered to both dorsal and lateral surfaces of hepatocytes.

E and EAC rosette-forming cells in healthy donors and cancer patients.

The influence of age and sex on the lymphocyte count and numbers of E and EAC rosette-forming cells (RFC) was investigated using peripheral blood of healthy donors. In the female donors we found a lower total lymphocyte count and percentage of EAC RFC than in male donors. The percentage and total number of E RFC appeared to be low in younger donors.