ArticleCancer prevention research (Philadelphia, Pa.)2014
Pubertal bisphenol A exposure alters murine mammary stem cell function leading to early neoplasia in regenerated glands.
Article in Cancer prevention research (Philadelphia, Pa.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 39 citations in OpenAlex.
- Bisphenol A and breast cancer: Can mechanistic plausibility be reconciled with epidemiological inconsistency?iScience · 2026Review
- Review
- Metformin reduces basal subpopulation and attenuates mammary epithelial cell stemness in FVB/N mice.Frontiers in cell and developmental biology · 2024Article
- Re-evaluation of the risks to public health related to the presence of bisphenol A (BPA) in foodstuffs.EFSA journal. European Food Safety Authority · 2023Article
- Bisphenol A replacement chemicals, BPF and BPS, induce protumorigenic changes in human mammary gland organoid morphology and proteome.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- In Utero Exposure to Bisphenol a Promotes Mammary Tumor Risk in MMTV-Erbb2 Transgenic Mice Through the Induction of ER-erbB2 Crosstalk.International journal of molecular sciences · 2020Article
- Fetal Alcohol Exposure Alters Mammary Epithelial Cell Subpopulations and Promotes Tumorigenesis.Alcoholism, clinical and experimental research · 2020Article
- Bisphenols and Risk of Breast Cancer: A Narrative Review of the Impact of Diet and Bioactive Food Components.Frontiers in nutrition · 2020Review
- Review
- Article
- Linking the Epigenome with Exposure Effects and Susceptibility: The Epigenetic Seed and Soil Model.Toxicological sciences : an official journal of the Society of Toxicology · 2017Review
- Low-Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2017Review
- Aging is associated with an expansion of CD49fAging · 2016Article
- Characterization of mammary epithelial stem/progenitor cells and their changes with aging in common marmosets.Scientific reports · 2016Article
- Epigenetics of breast cancer: Modifying role of environmental and bioactive food compounds.Molecular nutrition & food research · 2016Review
- Quantitative proteomic analyses of mammary organoids reveals distinct signatures after exposure to environmental chemicals.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- A review of the carcinogenic potential of bisphenol A.Reproductive toxicology (Elmsford, N.Y.) · 2016Review
- Article
- The dynamics of murine mammary stem/progenitor cells.Frontiers in biology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Perinatal exposure to bisphenol A (BPA) has been shown to cause aberrant mammary gland morphogenesis and mammary neoplastic transformation. Yet, the underlying mechanism is poorly understood. We tested the hypothesis that mammary glands exposed to BPA during a susceptible window may lead to its susceptibility to tumorigenesis through a stem cell-mediated mechanism. We exposed 21-day-old Balb/c mice to BPA by gavage (25 μg/kg/d) during puberty for 3 weeks, and a subset of animals were further challenged with one oral dose (30 mg/kg) of 7,12-dimethylbenz(a)anthracene (DMBA) at 2 months of age. Primary mammary cells were isolated at 6 weeks, and 2 and 4 months of age for murine mammary stem cell (MaSC) quantification and function analysis. Pubertal exposure to the low-dose BPA increased lateral branches and hyperplasia in adult mammary glands and caused an acute increase of MaSC in 6-week-old glands and a delayed increase of luminal progenitors in 4-month-old adult gland. Most importantly, pubertal BPA exposure altered the function of MaSC from different age groups, causing early neoplastic lesions in their regenerated glands similar to those induced by DMBA exposure, which indicates that MaSCs are susceptible to BPA-induced transformation. Deep sequencing analysis on MaSC-enriched mammospheres identified a set of aberrantly expressed genes associated with early neoplastic lesions in patients with human breast cancer. Thus, our study for the first time shows that pubertal BPA exposure altered MaSC gene expression and function such that they induced early neoplastic transformation.
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Registered trials
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