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Genetics of Colon Carcinogenesis in Mice Treated with 1,2-Dimethylhydrazine¹

Roswell Park Memorial Institute, Buffalo, New York 14263

Genetic analysis of colon tumor induction by symmetrical 1,2-dimethylhydrazine (DMH) was undertaken in F₁, F₂, and reciprocal backcross hybrids derived from a cross between two inbred mouse strains, the 100% susceptible ICR/Ha and completely resistant C57BL/Ha. Mice, 12 to 14 weeks old, received 22 successive weekly s.c. injections of 0.35% aqueous solution of DMH buffered to pH 6.5. A dose of 15 mg/kg/mouse/week produced invasive colon adenocarcinomas in all ICR/Ha males and females (60 of 60) within 22 weeks. None of the 90 C57BL/Ha mice developed DMH tumors during 44 weeks of observation. Susceptibility to the carcinogen was dominant, as indicated by 100% colon tumor incidence in reciprocal ICR/Ha x C57BL/Ha F₁ hybrids (68 of 68) and in the susceptible backcross ICR/Ha x F₁ (42 of 42). Tumor yield in F₂ hybrids (94 of 120) was 78%, which is in close agreement with the 3:1 ratio expected if a single dominant DMH susceptibility gene is inherited via the F₁ from the ICR/Ha grandparent. Likewise, tumor yield in resistant backcross mice of genotype C57BL/Ha x F₁ (46 of 117) is not out of line with the anticipated 1:1 ratio in the latter type of test hybrids. Tests with five isozyme markers and two coat color genes have tentatively ruled out linkage of DMH susceptibility on seven autosomes. The 47% tumor incidence among 57 male resistant backcross hybrids, regardless of whether their single X chromosome was inherited from the ICR/Ha or C57BL/Ha strain, provides evidence against sex linkage.

¹ Supported in part by Contract NIH-70-2035 from the Division of Cancer Treatment, National Cancer Institute, Bethesda, Md., and by NIH Grant HD05196 from Child Health and Human Development.

Received 7/26/76. Accepted 10/ 1/76.

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