title: Genetics of murine sarcoma virus (MSV)--induced tumors in AKR mice: Evidence that late progressing and early regressing tumors are controlled by different gents.
abstract: The genetics of late appearing MSV tumors showing a progressive growth pattern in AKR mice was investigated. The late MSV tumor response in F1 hybrids depended on the genetic background of the non-AKR parent. Within the 4-month observation period following virus injection, (CBA X AKR) F1, (DBA/2 X AKR)F1, and (NIH X AKR)F1 developed progressing MSV tumors, which exhibited latency and growth behavior comparable to that seen in AKR mice, (BALB X AKR)F1, (B6 X AKR)F1, and (B10br x akr)f1 mice did not show any late MSV tumors. In contrast to early regressing M-MSV tumors, whose development is independent of Fv-1 genotype, late MSV tumor progression is largely a function of this gene, since all late tumors which appeared in (B10BR x AKR) x AKR were observed in Fv-1n homozygous mice, H-2k halotype is a further factor in the occurrence of late MSV tumors, at least in (B6 x AKR) x AKR mice. In crosses of AKR with Fv-1 compatible mice, tumor appearance was strongly associated with inheritance of AKR-Mulv, and MSV recovered from late tumors of first back-cross animals appeared to be a new pseudotype with the endogenous AKR-MuLV. It is suggested that the host genetic control in both early and late MSV tumors is exerted mainly on the helper component of the leukemia-sarcoma complex.
mesh_terms: D000818:Animals; D000951:Antigens, Neoplasm; D000956:Antigens, Viral; D003433:Crosses, Genetic; D000939:Epitopes; D017988:Gammaretrovirus; D006650:Histocompatibility Testing; D006824:Hybridization, Genetic; D051379:Mice; D008806:Mice, Inbred AKR; D008815:Mice, Inbred Strains; D009053:Sarcoma Viruses, Murine; D012513:Sarcoma, Experimental / Q000235:genetics* / Q000276:immunology
chemical_list: D000951:Antigens, Neoplasm; D000956:Antigens, Viral; D000939:Epitopes