title: Enhancing effects of estrogens on endometrial carcinogenesis initiated by N-methyl-N-nitrosourea in ICR mice.
abstract: The present study was undertaken to examine the effects of estrogens, such as estrone (E1), 17 beta-estradiol (E2) and estriol (E3), on endometrial carcinogenesis initiated by N-methyl-N-nitrosourea (MNU) in mice. A total of 120 female ICR mice received MNU solution (1 mg/100 g body wt.) and normal saline at 10 weeks of age into their left and right uterine corpora, respectively. One week later, they were divided into four groups and treated as follows: Group 1 (30 mice) was given 25 ppm E1-containing diet; and Group 2 (30 mice) was fed 5 ppm E2-containing diet; Group 3 (30 mice) was given 25 ppm E3-containing diet; and Group 4 (30 mice) was fed the basal diet alone. At the termination of the experiment (Week 30), all surviving animals were autopsied and histopathological examinations revealed that endometrial adenocarcinomas had developed in all groups. The incidence of adenocarcinomas in the MNU-treated uterine corpus in Group 1 (25 ppm E1-feeding, 9/23, 39%) was significantly higher than that in Group 4 (basal diet, 3/26, 12%, P < 0.05). Also, the incidences of adenocarcinomas in the MNU-treated uterine corpus in Groups 2 (5 ppm E2-feeding, 8/24, 33%) and 3 (25 ppm E3-feeding, 7/26, 28%) were higher than in Group 4, but the difference was not statistically significant. Feeding of diet containing E1, E2 and E3 increased the incidences of the preneoplastic endometrial lesions (atypical, adenomatous or cystic glandular hyperplasia). In the uterine cervix, small numbers of squamous cell carcinomas, dysplasias or hyperplasias were occasionally found in all groups. These results indicate enhancing effects of the above three types of estrogens on the endometrial carcinogenesis induced by MNU in ICR mice.
authors.affiliation: Department of Obstetrics & Gynecology, Gifu University School of Medicine.
authors.forename: K
authors.initials: K
authors.lastname: Niwa
authors.forename: T
authors.initials: T
authors.lastname: Murase
authors.forename: T
authors.initials: T
authors.lastname: Furui
authors.forename: S
authors.initials: S
authors.lastname: Morishita
authors.forename: H
authors.initials: H
authors.lastname: Mori
authors.forename: T
authors.initials: T
authors.lastname: Tanaka
authors.forename: H
authors.initials: H
authors.lastname: Mori
authors.forename: T
authors.initials: T
authors.lastname: Tamaya
mesh_terms: D000230:Adenocarcinoma / Q000139:chemically induced* / Q000473:pathology; D000818:Animals; D004714:Endometrial Hyperplasia / Q000139:chemically induced / Q000473:pathology; D016889:Endometrial Neoplasms / Q000139:chemically induced* / Q000473:pathology; D004958:Estradiol / Q000494:pharmacology*; D004964:Estriol / Q000494:pharmacology*; D004970:Estrone / Q000494:pharmacology*; D005260:Female; D008770:Methylnitrosourea; D051379:Mice; D008813:Mice, Inbred ICR; D009929:Organ Size; D014599:Uterus / Q000473:pathology
chemical_list: D004970:Estrone; D004958:Estradiol; D008770:Methylnitrosourea; D004964:Estriol