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Br J Cancer. 1989 Feb;59(2):198-205.

Diploid nature of hepatocellular tumours developing from transplanted preneoplastic liver cells.

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Department of Tissue Culture, Institute for Cancer Research, Norwegian Radium Hospital, Oslo.


Hepatocyte suspensions were transplanted to the livers of syngeneic Wistar Kyoto rats by means of intraportal injection. Labelling of the donor cells with 51Cr or tritiated thymidine showed that 20% of the cells survived the transplantation procedure and were permanently retained by the recipient liver. Hepatocytes transplanted from normal livers produced no tumours, whereas donor cells from preneoplastic livers of rats treated with the carcinogens diethylnitrosamine and 2-acetylaminofluorene produced neoplastic nodules and hepatocellular carcinomas in the recipients. The number of tumours per host liver was proportional to the number of hepatocytes transplanted. Treatment of the host rats with phenobarbitone accelerated tumour development, causing liver cancer in the majority of the animals within three months. As opposed to the polyploid surrounding liver, both phenobarbitone-promoted and unpromoted host tumours contained predominantly (70-90%) diploid cells, regardless of the wide range of transplant ploidies (10-80% diploid cells) achieved by means of centrifugal elutriation. The results indicate that all host tumours arise from diploid donor hepatocytes and that the acquisition of a constitutive, predominantly non-polyploidising growth pattern may be a characteristic property of hepatocellular tumours.

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