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Tumorigenesis of mammary gland by 7,12 dimethylbenz( a )anthracene during pregnancy: Relationship with DNA synthesis
Author(s) -
Sinha Dilip K.,
Pazik James E.
Publication year - 1981
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910270612
Subject(s) - dmba , 7,12 dimethylbenz[a]anthracene , carcinogen , pregnancy , mammary gland , carcinogenesis , medicine , endocrinology , gestation , mammary tumor , lactation , fetus , biology , cancer , breast cancer , biochemistry , genetics
The relationship between mammary cell proliferation during pregnancy and susceptibility to 7,12‐dimethyl‐benz(a)anthracene (DMBA) was examined. DMBA was administered intravenously to Sprague‐Dawley rats on the 5th, 10th or 15th day of pregnancy. [ 3 H]thymidine labelling index (LI) of the mammary cells at the time of treatment with the carcinogen was determined and found to be higher in the pregnant rats than in agematched virgin controls. In spite of the high proliferative index of the mammary cells, significant inhibition of tumorigenesis occurred in the pregnant rats allowed to complete pregnancy and parturition following treatment with DMBA. However, when pregnancy was terminated by cesarian section shortly after treatment with DMBA, there was a significantly higher tumor incidence as compared to the ‘full‐term’ rats. It was observed that the earlier the pregnancy was terminated, the greater was the incidence of mammary tumors. This would indicate that the inhibitory effect of pregnancy is related to changes occurring during the later half of gestation. The differentiation of mammary cells for milk synthesis as pregnancy progresses is postulated to be a major reason for the observed refractoriness of the mammary cells to DMBA at that time.