Evaluation of the Carcinogenic Effects of Estrogens, Progestins and Oral Contraceptives on Cervix, Uterus and Ovary of Animals and Man

Drill, Victor A.

doi:10.1007/978-3-642-67265-1_5

Cited by 8 publications

(2 citation statements)

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“…Exposure to DES has been documented to be associated with abnormal differentiation and organization of the uterus (Couse and Korach 2004). Estrogen induces uterine carcinoma in mice, rabbits, and menopausal and postmenopausal women (Drill 1979). Exposure to estrogens in the fetal or newborn period can also induce uterine tumors in mice and rats (Kitamura et al 1999; Newbold, Bullock, and McLachlan 1990).…”

Section: Discussionmentioning

confidence: 99%

“…Exposure to estrogens in the fetal or newborn period can also induce uterine tumors in mice and rats (Kitamura et al 1999; Newbold, Bullock, and McLachlan 1990). Genistein, DES, and estrogen also induce a high incidence of uterine SM in rodents (Biegel et al 1998; Couse and Korach 2004; Drill 1979; Newbold et al 2001; Wordinger and Morrill 1985). Squamous cell carcinoma also appears subsequent to chronic exposure of mice to estrogen (Hart 1990).…”

Section: Discussionmentioning

confidence: 99%

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Reproductive Lesions in Female Harlan Sprague-Dawley Rats Following Two-Year Oral Treatment with Dioxin and Dioxin-like Compounds

et al. 2009

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Results from previously published animal studies suggest that prenatal and postnatal exposure to dioxin and dioxin-like compounds (DLCs) may profoundly affect the reproductive system of both sexes via endocrine disruption. In the present work, we evaluate the toxicity and carcinogenicity of various DLCs, with an emphasis on their effect on the reproductive organs, induced by chronic exposure of female adult Harlan Sprague-Dawley rats. This investigation represents part of an initiative of the National Toxicology Program to determine the relative potency of chronic toxicity and carcinogenicity of polychlorinated dioxins, furans, and biphenyls. For fourteen, thirty-one, or fifty-three weeks or for two years, animals were administered by gavage 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); 3,3',4,4',5-pentachlorobiphenyl (PCB126); 2,3,4,7,8-pentachlorodibenzofuran (PeCDF); 2,2',4,4',5,5'-hexachlorobiphenyl (PCB153); 2,3',4,4',5-pentachlorobiphenyl (PCB118); a tertiary mixture of TCDD, PCB126, and PeCDF; a binary mixture of PCB126 and 153; or a binary mixture of PCB126 and PCB118. The ranges of treatment-related changes in the reproductive system included chronic active inflammation in the ovary that occurred in the 1,000 and 3,000 microg/kg core groups (two-year exposure) of PCB153 and in the 300 ng/3,000 microg/kg core group of binary mixture of PCB126 and PCB153. Increases in the incidence of acute and/or chronic active inflammation of the uterus were observed in all dosed groups, including the stop-exposure group (withdrawal after thirty-week exposure) of PeCDF and the 1,000 microg/kg and/or higher group dosed with PCB153. The incidence of cystic endometrial hyperplasia was marginally increased in the 92 PeCDF ng/kg group at two years. The incidence of squamous metaplasia was significantly increased in the 44 ng/kg and higher dose group, including the stop-exposure group. The incidence of uterine squamous cell carcinoma was significantly or marginally increased in the 6 ng/kg core and 100 ng/kg stop-exposure groups of TCDD and in the 300 ng/300 microg/kg core group that received the binary mixture of PCB126 and 153. The incidence of uterine carcinoma was marginally increased in the 92 ng/kg PeCDF group at two years and clearly increased in the 1,000 and 4,600 microg/kg PCB118 core group and the 4,600 microg/kg stop group. In the studies of PCB 126, the tertiary mixture, and the binary mixture of PCB126 and PCB118, no increased incidence of any change occurred in the reproductive systems. The range of changes seen with the different compounds suggests that more than one mechanism may have been involved in promoting the female reproductive pathology.

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