The genetics of late appearing MSV tumors showing a progressive growth pattern in AKR mice was investigated. The late MSV tumor response in F 1 hybrids depended on the genetic background of the non-AKR parent. Within the 4-month observation period following virus injection, (CBAxAKR)F 1, (DBA/2xAKR)F 1, and (NIHxAKR)F 1 developed progressing MSV tumors, which exhibited latency and growth behavior comparable to that seen in AKR mice. (BALBxAKR)F 1, (B6xAKR)F 1, and (B10BRxAKR)F 1 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 (B10BRxAKR)xAKR were observed in Fv-1(n) homozygous mice. H-2(k) haplotype is a further factor in the occurrence of late MSV tumors, at least in (B6xAKR)xAKR 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.
|Number of pages||11|
|Journal||International Journal of Cancer|
|Publication status||Published - 1977|
ASJC Scopus subject areas
- Cancer Research