The growth pattern (progression/regression) of v-src DNA- and Rous sarcoma virus (RSV)-induced tumors was analogous on a panel of inbred chicken lines. The decisive role of the major histocompatibility complex [Mhc(B)] alleles in resistance to the progression of these tumors was formally proved in segregating backcross populations. The immune mechanism of tumor regression was demonstrated by both in vivo and in vitro assays. A protective effect of v-src-specific immunity against RSV challenge was shown in Rous sarcoma regressor, line CB (B12/B12). Immune cells from regressors of v-src DNA-induced tumors can protect syngeneic hosts from the development of tumor after challenge with both v-src DNA and RSV. Suppression of RSV-induced tumor cell growth in vitro was also achieved by the use of cocultivation with spleen cells from chickens in which v-src DNA-induced tumors had regressed. This in vitro sarcoma-specific response was Mhc(B)-restricted. Chickens of the congenic Rous sarcoma progressor line CC (B4/B4) are sometimes able to regress v-src DNA-induced tumors, but immune cells can only slow the growth of v-src DNA-induced tumors in syngeneic hosts. This suggests that the primary reason for the susceptibility of CC chickens is a weak v-src-specific immune response. Furthermore, some of the v-src DNA-induced tumors were transplantable across the Mhc(B) barrier. The growth of tumor allografts was able to be facilitated when immunological tolerance to the B-F/L region antigens (class I and class II) had been established. This demonstrated that a high tumorigenicity of the transplantable tumor was not due to the lack of Mhc(B) antigens on tumor cells.

• MeSH
• DNA, Viral genetics   MeSH
• Neoplasms, Experimental immunology   MeSH
• Genes, src * MeSH
• Major Histocompatibility Complex * MeSH
• Inbreeding MeSH
• Chickens immunology   MeSH
• Oncogene Protein pp60(v-src) immunology   MeSH
• Repetitive Sequences, Nucleic Acid MeSH
• Cell Transformation, Viral MeSH
• Avian Sarcoma Viruses genetics   MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• DNA, Viral MeSH
• Oncogene Protein pp60(v-src) MeSH

• MeSH
• Crossing Over, Genetic * MeSH
• Genotype * MeSH
• Haplotypes MeSH
• Major Histocompatibility Complex genetics   MeSH
• Chickens MeSH
• Polymorphism, Restriction Fragment Length MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Journal Article MeSH

We report that the cloned DNA harboring the long terminal repeat (LTR), v-src, LTR proviral structure is tumorigenic in chickens of the Prague congenic lines. The growth rate of these tumors is by far the highest in the recombinant CC.R1 line, the B haplotype of which is composed of the B-F/L4 and B-G12 subregions originating from different naturally occurring haplotypes. Some of the tumors induced by the LTR, v-src, LTR DNA are repeatedly transplantable in syngeneic chickens, maintain unaltered provirus, and express v-src mRNA. Differences in the response to challenge with Rous sarcoma virus (RSV) and LTR, v-src, LTR DNA on a given experimental model are compared and possible involvement of an interaction between B-F/L and B-G region genes is considered. Regression of the LTR, v-src, LTR DNA-induced tumors did not prevent the formation and growth of tumors induced subsequently by RSV.

• MeSH
• Cell Division genetics   MeSH
• DNA, Neoplasm physiology   MeSH
• Genes, src physiology   MeSH
• Cloning, Molecular MeSH
• Chickens MeSH
• Neoplasms genetics   microbiology   MeSH
• Blotting, Northern MeSH
• Polymorphism, Restriction Fragment Length MeSH
• Proviruses MeSH
• Repetitive Sequences, Nucleic Acid physiology   MeSH
• Blotting, Southern MeSH
• Genetic Complementation Test MeSH
• Avian Sarcoma Viruses MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• DNA, Neoplasm MeSH