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Spontaneous regression of friend‐virus‐induced erythroleukemia. VII. The genetic control of regression
Author(s) -
Dietz Michael,
Fouchey Susan,
Furmanski Philip
Publication year - 1981
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910270313
Subject(s) - biology , genetics , allele , gene , genotype , regression , strain (injury) , inbred strain , penetrance , microbiology and biotechnology , phenotype , psychology , anatomy , psychoanalysis
The genetic control of spontaneous regression of erythroleukemia was studied in parental and hybrid mice in which leukemia was induced by the regressing strain of Friend virus (RFV). Because in previous studies parental regressor mouse strains tested (N/PLCR, SIM, NIH Swiss) all had the Fv‐I n/n genotype and the progressor mouse strains (SIM.R, 3ALB/c) had the Fv‐I b/b genotype, we determined the influence of Fv‐I alleles on regression. Genes which influence regression were dominant and had partial penetrance in (progressor X regressor) F 1 mice. Regression occurred in hybrid mice which inherited the Fv‐I b/b genes of each of the progressor mouse strains. Regression and Fv‐I alleles also segregated independently in (N/PLCR X BALB/c) F 2 mice, in random‐bred Swiss mice heterozygous for the Fv‐I gene, in partially inbred Swiss recombinant progressor and regressor mouse lines, and in hybrid mice carrying the Fv‐I b/b gene of SIM.R mice. Regressor SIM and progressor SIM.R mice, which were bred to be congeneic at the Fv‐I locus, also differ with respect to recovery from viremia, suggesting that their Rfv‐3 genes differ and influence regression. Crosses of SIM and SIM.R mice with the A.BY ( Rfv‐3 s/s ) mouse strain confirmed that SIM and SIM.R carry Rfv‐3 r/r and Rfv‐3 s/s , respectively. We conclude that Fv‐I b/b is not inhibitory to regression nor is the Fv‐I gene a genetic determinant in the process. The data suggest that regression is influenced by several genes, including those ( Rfv‐1, Rfv‐2, Rfv‐3 ) shown to affect recovery from leukemia in other systems.