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Departments of Radiation Oncology [C. G., A. S., A. A., G. R. G., B. V.], Medicine [S. Gu., S. Ga., R. S., N. R-C., J. R-C.], Pathology [K. E. T.], and Molecular Genetics [N. R-C., J. R-C.] and The Marion Bessin Liver Research Center [S. Gu., S. Ga., R. S., N. R-C., J. R-C.], Albert Einstein College of Medicine, Bronx, New York 10461, and Department of Radiation Oncology, Beth Israel Medical Center, New York, New York [A. A.]
Hepatic tumors often recur in the liver after surgical resection. Postoperative radiotherapy (RT) could improve survival, but curative RT may induce delayed life-threatening radiation-induced liver damage. Because RT inhibits liver regeneration, we hypothesized that unirradiated, transplanted hepatocytes would proliferate preferentially in a partially resected and irradiated liver, providing metabolic support. We subjected F344 rats to hepatic RT and partial hepatectomy with/without a single intrasplenic, syngeneic hepatocyte transplantation. Hepatocyte transplantation ameliorated radiation-induced liver damage and improved survival of rats receiving RT after partial hepatectomy. We further demonstrated that transplanted hepatocytes extensively repopulate and function in a heavily irradiated rat liver.
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