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Cell Genetics Laboratory, Department of Obstetrics and Gynecology, and Division of Allergy and Immunology, Department of Medicine, Cornell University Medical College, New York, New York 10021
B16 mouse melanoma cells (clone B559) grown in 1 to 3 µg of 5-bromodeoxyuridine (BUdR) per ml form few or no tumors in C57BL/6J adult mice when injected subcutaneously in doses at which untreated cells always form tumors. Injections of BUdR-grown cells protect adult mice against melanoma. Melanoma cells grown in 1 µg of BUdR per ml for almost 1 year (clone C3471) retain a plating efficiency similar to that of untreated cells. When C3471 cells are injected into C57BL/6J mice treated with antithymocyte serum or into neonates, tumors grow and kill all the mice. Melanoma cells grown in 3 µg of BUdR per ml for 14 days form no tumors in normal adult mice, but form tumors and kill 72% of antithymocyte serum-treated adults and 21% of neonates inoculated with 106 cells. Although their plating efficiency is reduced from control levels, the ability of BUdR-treated melanoma cells to grow in vivo is proved by tumor formation in immunologically compromised mice. Growth in both concentrations of BUdR greatly increases production of a C-type virus. C3471 cells express Gross cell surface antigen, undetectable in control cells, and increase their expression of H-2b antigen. The ability of BUdR-grown cells to protect against melanoma and to form tumors in neonates and antithymocyte serum-treated adults, in contrast to normal adults, and their increased production of virus and of cell surface antigens, all make it likely that one component of the loss of tumorigenicity is a change in antigenicity of these cells.
1 This work was supported by USPHS Grants CA 10095 and CA 13339, by Damon Runyon Grant 1095, and by grants from the New York Cancer Research Institute, Inc., and from the Irwin Strasburger Memorial Medical Foundation.
2 Recipient of Faculty Research Award PRA-77 from the American Cancer Society.
Received 6/13/73. Accepted 9/28/73.
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