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Cell Population Growth and Cell Loss in the MTG-B Mouse Mammary Carcinoma¹

Radiobiology Laboratories, Departments of Radiology and Pathology, University of Wisconsin Medical School, Madison, Wisconsin 53706

Two radiobiochemical methods were used in studies of tumor cell population growth rate and cell loss during growth of grafts of C3H mouse mammary carcinoma MTG-B in BC3F₁ mice. Six-hr uptake of orotic acid-5-³H into DNA and RNA was highest in small tumors (25 mg, Day 5 after grafting). RNA uptake fell to one-third maximum by Day 7 and DNA reached that point by Day 9, thereafter remaining constant until Day 16 (1200-mg tumors). Tumor DNA was prelabeled with multiple injections of either tritiated thymidine or 5-iodo-2'-deoxyuridine-¹²⁵I given prior to the first day of sacrifice. The specific activity of tritiated thymidine-labeled DNA fell exponentially from Days 5 through 10 and then tended to plateau. 5-Iodo-2'-deoxyuridine-¹²⁵I-labeled DNA specific activity decreased similarly until Day 13, and slowed thereafter. In all experiments, the growth rate of "cleaned" viable tumor tissue decreased as tumors became larger. It is postulated that: (a) the rate of decrease in ¹²⁵I-labeled tumor DNA specific activity is the negative of the "potential" cell population growth rate exclusive of cell death; (b) the potential rate of cell population growth is constant in tumors weighing 22 to 1200 mg or more; (c) cell death rate disproportionately increases in large tumors; and (d) tritiated thymidine released from dying cells is reutilized more efficiently than 5-iodo-2'-deoxyuridine-¹²⁵I. These data are consistent with the postulate that increased cell death and decreased nucleic acid synthetic activity result from the known decrease in functional vascular space relative to tumor size. Evidence for the constancy in rate of cell population increase during tumor latency is also presented.

¹ Project supported in part by American Cancer Society Grant T661 and National Cancer Institute Grant CA-08318.

² Supported in part from Radiotherapy Center Grant Ca-06295, National Cancer Institute, USPHS.

³ Research Career Development Awardee CA-38655.

Received 1/15/69. Accepted 8/ 1/69.