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Xenotropic Virus Expression and Susceptibility to 3-Methylcholanthrene-induced Cancer¹

Geomet Technologies, Inc., 6000 Executive Boulevard, 4th Floor, Bethesda, Maryland 20852 [K. T. N.]; Department of Biochemical Oncology, Microbiological Associates, Inc., Bethesda, Maryland 20016 [B. O., R. E. K.]; and Cancer Research Institute, University of California School of Medicine, San Francisco, California 94143 [J. A. L.]

This paper reports the lack of genetic linkage between spontaneous production of substantial amounts of infectious xenotropic (X-tropic) virus and the susceptibility to chemically induced cancers in two inbred strains of mice, NZB/BLNJ and 129/J, and their genetic crosses. The parental strains and F₁, backcross, and F₂ progeny between these two strains were partially splenectomized to ascertain X-tropic viral status and were subsequently treated s.c. with 500 µg of 3-methylcholanthrene in trioctanoin. Progeny from second backcrosses [(F₁ x 129) x 129] were also tested for their X-tropic viral status and susceptibility to 3-methylcholanthrene carcinogenesis. Mice were observed for evidence of fibrosarcomas at the site of inoculation over a 10-month period. In this genetic system, spontaneous production of high titers of X-tropic virus segregated as a single autosomal dominant gene. Susceptibility to 3-methylcholanthrene-induced fibrosarcomas did not segregate in these crosses, and susceptibility did not correlate with the degree of X-tropic virus expression.

¹ This work was supported by a contract to Microbiological Associates, Bethesda, Md., from the Council for Tobacco Research, U. S. A. Presented in part at the 78th Annual Meeting of the American Society for Microbiology, May 1978, Las Vegas, Nev.

² To whom requests for reprints should be addressed.

³ Recipient of Grant 1011 from the Council for Tobacco Research, U. S. A., and Research Career Development Award CA 70990 from the National Cancer Institute.

Received 1/29/80. Accepted 8/15/80.