A locus that influences susceptibility to 1, 2-dimethylhydrazine-induced colon tumors maps to the distal end of mouse chromosome 3.

While inheritance of mutated alleles of highly penetrant tumor suppressor genes such as retinoblastoma or p53 predisposes individuals to a greatly increased risk of developing cancer, epidemiological data indicate that the majority of sporadic tumors in humans result from interactions of environmental and host genetic factors. The host genetic factors are poorly penetrant tumor susceptibility genes that determine the likelihood that a cancer will arise from carcinogen exposure. The majority of colon tumors in humans are sporadic in nature.

1,2-Dimethylhydrazine carcinogenesis in C3HA and CBA female mice prenatally treated with diethylstilbestrol.

C3HA and CBA female mice received a single intraperitoneal (i.p.) injection of 0.

[The effect of prenatal diethylstilbestrol treatment on 1,2-dimethylhydrazine-induced carcinogenesis in C3HA female mice].

C3HA female mice received 0.1-0.3 mg/g body weight diethylstilbestrol (DES) on day 17 of gestation.

[1,2-dimethylhydrazine induction of epithelial tumors of the kidneys in CBA strain mice].

The results of experiments on the 1,2-dimethylhydrazine (DMH) induction of epithelial renal tumours in CBA male mice are presented. The dose-response study shows a sharp increase (from 5 to 75%) of the epithelial renal tumour incidence in the range of 2, 4 and 8 injections of DMH. Higher doses induce a decrease of the tumour incidence due to the early death caused by other tumours.

Carcinogenicity of deuterium-labeled 1,2-dimethylhydrazine in mice.

To study the effect of deuterium substitution on the carcinogenicity of 1,2-dimethylhydrazine (DMH) in mice, two comparisons were made between DMH and its fully methyl-deuterated analogue, [2H6]DMH. In a lifetime study with the CBA strain, groups of 19-30 animals of each sex were dosed s.c.