H-2-controlled Genetic Susceptibility to Pulmonary Adenomas Induced by Urethane and 4-Nitroquinoline 1-Oxide in A/Wy Congenic Strains

Abstract

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-2^a), A/J (H-2^a), A.TL (H-2^t1) and A.AL (H-2^a1) than in A.BY (H-2^b), A.SW (H-2^a), A.CA (H-2^t) and A.TH (H-2^t2) strains. In addition, the average number of adenoma foci in A/Wy (H-2^a) was more than 20 times that in the B10.A (H-2^a) 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.