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Carcinogenesis, Vol. 21, No. 5, 1039-1042, May 2000
© 2000 Oxford University Press

Carcinogenesis

Rapid induction of uterine tumors with p53 point mutations in heterozygous p53-deficient CBA mice given a single intraperitoneal administration of N-ethyl-N-nitrosourea

Kunitoshi Mitsumori2, Hiroshi Onodera, Takeo Shimo, Kazuo Yasuhara, Hisayoshi Takagi, Takatoshi Koujitani, Masao Hirose, Chika Maruyama1 and Shigeharu Wakana1

Division of Pathology, National Institute of Health Sciences, 1-18-1, Kamiyoga, Setagaya-ku, Tokyo 158-8501 and
1 Central Institute for Experimental Animals, 430 Nogawa, Miyamae-ku, Kawasaki 216-0001, Japan

To investigate the sensitivity of heterozygous p53-deficient CBA mice to carcinogens, 20 female mice [p53(+/–)] and 20 wild-type littermates [p53(+/+)] were given an intraperitoneal injection of 120 mg/kg body wt of N-ethyl-N-nitrosourea (ENU) and were maintained without any other treatment for a further 26 weeks. Histopathology showed that uterine tumors (endometrial polyps and stromal sarcomas) and lung adenomas were induced in both p53(+/–) and p53(+/+) mice. The incidence of uterine tumors and lung adenomas (94% and 81%, respectively) in p53(+/–) mice was significantly greater than that in p53 (+/+) mice (37% and 42%, respectively). Malignant lymphomas were only induced in p53(+/–) mice, at an incidence of 31%. Concerning uterine tumors and preneoplastic lesions, there were endometrial stromal sarcomas and atypical hyperplasias of the endometrial gland in 90% and 63%, respectively, of p53(+/–) mice, with significantly greater incidences than in p53(+/+) mice. Gene analysis revealed GCG->GTG point mutations in codon 135 of exon 5 of the p53 allele in all of the uterine endometrial stromal sarcomas examined. Our results suggest that female p53(+/–) CBA mice are very susceptible to uterine carcinogenesis, providing a useful model for ENU-induced uterine tumors.


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