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Genetic Determination of Differential Inflammatory Reactivity and Subcutaneous Tumor Susceptibility of AKR/J and C57BL/6J Mice to 7,12-Dimethylbenz[a] anthracene¹

Division of Experimental Chemotherapy, Sloan-Kettering Institute for Cancer Research, New York, New York 10021

Since previous work has shown that 7,12-dimethylbenz[a]-anthracene (DMBA) causes less inflammation in AKR/J than in C57BL/6J mice, the genetic nature of this differential inflammatory response was investigated. The criterion for high reactivity was the formation of ulcers after skin application of DMBA. F₁ hybrids were slightly less high reacting than the C57BL/6J mice. Of the F₂, 72% were high reacting. The back-cross of F₁ hybrids to C57BL/6J produced only high reactors, but to AKR/J high- and low-reacting mice. Mating of low-reacting F₁ backcross mice to C57BL/6J mice yielded 100%, and to AKR/J 0%, high reactors. Backcross of low-reacting F₂ mice to C57BL/6J gave 100%, and to AKR/J 0%, high-reacting mice. Backcross of high-reacting F₁ backcross and F₂ mice to C57BL/6J yielded only high-reacting, and to AKR/J high- and low-reacting, mice. These findings suggest that the low inflammatory response of the AKR/J mice is controlled by a single incompletely recessive factor. Results with DBA/2J mice, their F₁ hybrids, and backcrosses of these F₁ hybrids to AKR/J, also indicated inheritance by a single autosomal genetic factor. The higher inflammatory reactivity of the C57BL/6J mice was accompanied by higher susceptibility to subcutaneous tumor induction by DMBA. Furthermore, results with mice differing only in inflammatory reactivity showed that inflammatory reactivity and susceptibility to s.c. tumor induction are inherited together and are probably directly related.

¹ This study was supported by National Cancer Institute Grant CA 08748.

Received 12/ 6/68. Accepted 4/ 7/69.