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Effect of Fast-growing Transplantable Hepatoma on Cell Proliferation in Host Tissue of the Mouse¹

Department of Anatomy, The University of Texas Medical School at San Antonio, San Antonio, Texas 78229

The effects of a transplanted hepatoma on cell proliferation in various cell populations of the host liver, spleen, kidney, ear, and tongue of male and female A/J mice were investigated. We utilized both biochemical and radioautographic procedures in order to quantitate the effects of the tumor on whole-organ DNA content and DNA synthesis and to define the particular cell populations in those organs that were primarily affected by the tumor. Greater than twofold increases in DNA content and DNA synthesis (as indicated by ³H-labeled thymidine incorporation into DNA) were observed in the spleens of tumor-bearing male and female mice; these observations support those of other investigators. Increases in DNA content and synthesis also were observed in the livers of tumor-bearing animals. Radioautographic analyses showed an increase in the percentage of labeled hepatocytes and nonhepatocytes (including sinusoidal lining and Kupffer cells) in these livers. An increase in labeled leukocytes was also observed in the tissue spaces of the livers of tumor-bearing animals. The kidneys of the tumor-bearing animals showed a substantial increase in DNA synthesis, due primarily to an increase in the turnover rate of the endothelial cells. A new finding in this study was that in tumor-bearing animals, some cell populations (such as the ear epidermis and the ventral tongue epithelium) decrease in proliferation and turnover in tumor-bearing animals at the same time that other cell populations in other tissues increase. These results show that the host-tumor interaction is complex and cannot be explained solely by an immunological reaction or a nutritional deficiency. One must consider a combination of at least these two factors in order to understand the effects of the tumor on the host.

¹ This work was supported in part by American Cancer Society Grant IN-90C, Subgrant 1-C; National Science Foundation Grant GB31580; and Morrison Trust R-A-33.

Received 6/ 2/72. Accepted 11/16/72.