V-onc mutation associated with host cell growth in retroviral tumors.

In sarcomagenesis in rats infected neonatally with feline sarcoma virus (ST-FeSV), v-fes product (P85) was previously shown by us to be a predictive and preventive determinant. In order to explore the part played by P85 in tumor suppression, DNA was extracted from precancerous granulomas and from slow or rapid growing sarcomas induced by neonatal injection of the virus. The v-fes signal from extracted DNA was analyzed by PCR-SSCP. The prototype v-fes gene signal was detected in most lesions and found to be generally amplified in rapid growing sarcomas and in some granulomas. Several v-fes homologs showing varying mobilities in gel were seen in most sarcomas and some granulomas with or without the prototype v-fes signal. In slow growing sarcomas and granulomas induced in hosts that were immunized with ST-FeSV induced syngeneic sarcoma and proved to carry IgG antibody to P85, the prototype v-fes gene was found to be down-regulated and v-fes homologs were found to be reduced in number or eliminated. These results suggest that the development of v-fes mutations is associated with the growth potential of cells carrying the v-fes gene, and that host immunity to v-onc product influences the development of virogene rearrangements and results in slow and suppressed growth of tumors caused by neonatal infection with retrovirus.