H-2-controlled genetic susceptibility to pulmonary adenomas induced by urethane and 4-nitroquinoline 1-oxide in A/Wy congenic strains.

The genetic effect of the H-2 complex on the development of chemically induced pulmonary adenomas was clearly demonstrated in H-2 congenic strains with an A/Wy background which had a high susceptibility to pulmonary adenoma. A single subcutaneous injection of either urethane or 4-nitroquinoline 1-oxide was given to nine strains of mice. Among them, the number of adenoma foci per mouse was significantly higher in A/Wy (haplotype H-2a), A/J (H-2a), A.TL (H-2tl) and A.AL (H-2al) than in A.BY (H-2b), A.SW (H-2s), A.CA (H-2f) and A.TH (H-2t2) strains. In addition, the average number of adenoma foci in A/Wy (H-2a) was more than 20 times that in the B10.A (H-2a) strain. Thus, multiplicity of adenoma foci appeared to be regulated by at least two genes, one of which is located in the I or S region in the H-2 complex and the other in the non-H-2 genetic background. The genes in the H-2 complex were distinct from Pas-1 locus, which is probably identical to ptr.