17β-oestradiol and Enovid mammary tumorigenesis in C3H/HeJ female mice: counteraction by concurrent 2-bromo-α-ergocryptine

Welsch, C W; Adams, C. E.; Lambrecht, Linda K.; Hassett, Clare; Brooks, Charles L.

doi:10.1038/bjc.1977.46

Cited by 20 publications

(2 citation statements)

References 22 publications

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“…86 Although it is not possible to directly establish the carcinogenic potential of OCs in the human breast in vivo, animal studies suggest that the hormones contained in OCs have carcinogenic potential in rodents, dogs, and monkeys. [87][88][89][90][91][92] Moreover, OCs accelerate the rate of breast cell division in women who take them before FFTP. 93 Increased rates of cell division are associated with increased cancer risk.…”

Section: Cases/controlsmentioning

confidence: 99%

Oral Contraceptive Use as a Risk Factor for Premenopausal Breast Cancer: A Meta-analysis

Kahlenborn

Modugno

Potter

et al. 2006

Mayo Clinic Proceedings

190

101

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Section: Cases/controlsmentioning

confidence: 99%

Oral Contraceptive Use as a Risk Factor for Premenopausal Breast Cancer: A Meta-analysis

Kahlenborn

Modugno

Potter

et al. 2006

Mayo Clinic Proceedings

190

101

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“…Chronic elevation of estrogens (9)(10)(11) or prolactin (12,13) increases the incidence and decrease the onset time of mammary tumors in either SD or F-344 rats. As such, treatment with agents that increase chronic secretion of estrogens and/or prolactin would be expected to increase the occurrence of mammary tumors in these strains.…”

Section: Endocrine Factors That Enhance the Growth Of Mammary Tumorsmentioning

confidence: 99%

Role of Strain-Specific Reproductive Patterns in the Appearance of Mammary Tumors in Atrazine-Treated Rats

Simpkins

Eldridge

Wetzel³

1998

ACS Symposium Series

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Atrazine has been a major agricultural herbicide in the U.S. for more than 25 years. It is used for the control of broadleaf and grass weeds in corn and sorghum crops. Because of its common use, the toxicity of atrazine has been the subject of many studies. Atrazine is not toxic with acute administration, with an oral and dermal LD 50 of greater than 3,000 mg/kg. In tests of mutagenicity, atrazine have been negative in more than 50 tests (1). Atrazine is not a teratogen or a reproductive toxin, and lacks carcinogenic activity in male and female mice and Fischer 344 (F-344) rats, as well as in male Sprague-Dawley (SD) rats. Five tests of the tumorogenicity of atrazine in SD rats have been conducted since the 1960s. Two of these tests, which assessed atrazine at doses up to 500 ppm, produced negative results, while 3 other studies have shown an earlier time of onset and/or an increased incidence of mammary tumors (2-4). With the exception of one study (4), the earlier onset of mammary tumors occurred at doses ≥ a maximum tolerated dose (2,3). A no-observed-effect-level (NOEL) for tumorogenicity was established in all studies.Atrazine is not a mutagen (1), a direct acting carcinogen and it has no intrinsic estrogenic activity (5,6).The increased incidence and/or earlier age of appearance of mammary tumors in female SD, but not Fischer 344 rats warrants an evaluation of the strainspecificity of this response. The results discussed here present strong evidence that the specificity of the tumor-enhancing effects of atrazine in the female SD rat are the result of a treatment-related earlier appearance of persistent estrus in that strain.

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Inhibition of mammary tumorigenesis in GR mice with 2‐bromo‐α‐ergocryptine

Welsch

Goodrich-Smith

Brown

et al. 1979

Intl Journal of Cancer

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A high incidence of mammary tumors is found in multiparous GR mice during the 2nd and 3rd pregnancies and in nulliparous GR mice treated with estrone/progesterone. The purpose of this study was to determine if prolactin is a contributing hormone in the genesis of these neoplasms. In one series of experiments, 238 15-week-old nulliparous GR mice were treated with estrone (drinking water, 0.5 mg/liter) plus progesterone (30 mg progesterone pellet with cholesterol, implanted SC once monthly) for a period of 13 weeks. Half of these mice were injected SC once daily with 100 micrograms of the prolactin-suppressing drug 2-bromo-alpha-ergocryptine (CB-154) for the duration of hormone treatment, and the other half were injected SC once daily with 0.9% NaCl solution (controls). In another series of experiments, 87 pregnant GR mice were divided into two groups and injected SC once daily from day 7 to 21 of pregnancy with 0.9% NaCl solution (controls) or CB-154 (100 micrograms/mouse). In the first series, the numbers of mice with mammary tumors and total number of mammary tumors were: controls, 58/119 (49%) and 73; CB-154 treatment, 34/119 (29%) and 37, respectively. In the second series, the numbers were: controls, 39/44 (89%) and 73; CB-154 treatment, 24/43 (56%) and 43, respectively. In both studies, CB-154 treatment significantly (p less than 0.05-0.005) reduced the percentage of mice with mammary tumors and total number of mammary tumors. These results provide evidence that prolactin is a contributing hormone in the genesis of estrone/progesterone and pregnancy-induced mammary tumors in female GR mice.

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17β-oestradiol and Enovid mammary tumorigenesis in C3H/HeJ female mice: counteraction by concurrent 2-bromo-α-ergocryptine

Cited by 20 publications

References 22 publications

Oral Contraceptive Use as a Risk Factor for Premenopausal Breast Cancer: A Meta-analysis

Oral Contraceptive Use as a Risk Factor for Premenopausal Breast Cancer: A Meta-analysis

Role of Strain-Specific Reproductive Patterns in the Appearance of Mammary Tumors in Atrazine-Treated Rats

Inhibition of mammary tumorigenesis in GR mice with 2‐bromo‐α‐ergocryptine

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