ArticleAlcoholism, clinical and experimental research2016
Tumor Phenotype and Gene Expression During Early Mammary Tumor Development in Offspring Exposed to Alcohol In Utero.
Article in Alcoholism, clinical and experimental research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Fetal Alcohol Exposure Alters Mammary Epithelial Cell Subpopulations and Promotes Tumorigenesis.Alcoholism, clinical and experimental research · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAlcohol exposure in utero increases susceptibility to carcinogen-induced mammary tumorigenesis in adult offspring and causes tumors with a more malignant phenotype. This study was conducted to identify changes early in tumor development that might lead to this outcome.
methodsPregnant Sprague-Dawley rats were fed a liquid diet containing 6.7% ethanol (alcohol), an isocaloric liquid diet without alcohol (pair-fed), or rat chow ad libitum (ad lib) from gestation day 7 until parturition. At birth, female progeny were cross-fostered to control dams. Pups were weaned at postnatal day (PND) 21 and fed rat chow ad libitum for the remainder of the experiment. Female offspring were administered N-nitroso-N-methylurea (NMU; 50 mg/kg body weight) on PND 50. Mammary glands were palpated weekly, and offspring were euthanized at 16 weeks post-NMU injection.
resultsAt 16 weeks post-NMU, tumor multiplicity was greater in alcohol-exposed offspring compared with control groups. Estrogen receptor-α (ER) mRNA expression was decreased in tumors from alcohol-exposed offspring, and these animals developed more ER-negative tumors relative to the pair-fed group. Alcohol-exposed offspring also tended to develop more progesterone receptor (PR)-positive tumors. All tumors were HER2-negative. PR positivity was associated with higher Ki67 expression, suggesting that PR-positive tumors were more proliferative. Tumors from alcohol-exposed animals exhibited increased mRNA expression of the insulin-like growth factor (IGF) family members IGF-II and IGFBP-5. IGF-II and DNA methyltransferase mRNA tended to be greater in the normal contralateral mammary glands of these animals.
conclusionsThese data indicate that alcohol exposure in utero may shift NMU-induced tumor development toward a more aggressive phenotype and that alterations in IGF-II expression may contribute to these changes. Additional studies should be aimed at epigenetic mechanisms that underlie IGF-II expression to further delineate how this gene is altered in mammary glands of adults exposed to alcohol in utero.
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