ArticleNature communications2020
Pregnancy reprograms the epigenome of mammary epithelial cells and blocks the development of premalignant lesions.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- Dynamics, function, and regulation of mammary stem cells in development and disease.Experimental & molecular medicine · 2026Review
- Branching out: the diverse roles of stem and progenitor cells in mammary gland development.Journal of mammary gland biology and neoplasia · 2026Review
- Estrogen metabolism pathways in pregnancy and subsequent breast cancer risk: a prospective follow-up study.Breast cancer research : BCR · 2026Article
- Association between childbirth history and multiple health outcomes.Archives of medical science : AMS · 2026Article
- Article
- Estrogen Metabolism Pathways in Pregnancy and Subsequent Breast Cancer Risk: A Prospective Follow-up Study.Research square · 2025Article
- Parity and NIS Expression in Atypical Cells of Triple-Negative Breast Cancer, and Prognosis.International journal of molecular sciences · 2025Article
- MaGNet: A Network-Based Method for Quantitative Analysis of the Mammary Ductal Tree in Developing Female Mice.Journal of mammary gland biology and neoplasia · 2025Article
- Article
- Understanding Susceptibility to Breast Cancer: From Risk Factors to Prevention Strategies.International journal of molecular sciences · 2025Review
- Maternal Diet Quality in Pregnancy and Human Milk Extracellular Vesicle and Particle microRNA.Epigenetics reports · 2025Article
- Comprehensive single-cell aging atlas of healthy mammary tissues reveals shared epigenomic and transcriptomic signatures of aging and cancer.Nature aging · 2025Article
- Brca1 haploinsufficiency promotes early tumor onset and epigenetic alterations in a mouse model of hereditary breast cancer.Nature genetics · 2024Article
- Organoid Cultures for the Study of Mammary Biology and Breast Cancer: The Promise and Challenges.Cold Spring Harbor perspectives in medicine · 2024Review
- Different Oncogenes and Reproductive Histories Shape the Progression of Distinct Premalignant Clones in Multistage Mouse Breast Cancer Models.The American journal of pathology · 2024Article
- Advanced 3D imaging and organoid bioprinting for biomedical research and therapeutic applications.Advanced drug delivery reviews · 2024Review
- Periconceptional and Prenatal Exposure to Metals and Extracellular Vesicle and Particle miRNAs in Human Milk: A Pilot Study.Exposure and health · 2023Article
- Three-dimensional genome architecture coordinates key regulators of lineage specification in mammary epithelial cells.Cell genomics · 2023Article
- Luminal Rank loss decreases cell fitness leading to basal cell bipotency in parous mammary glands.Nature communications · 2023Article
- Gestational Breast Cancer - a Review of Outcomes, Pathophysiology, and Model Systems.Journal of mammary gland biology and neoplasia · 2023Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Pregnancy causes a series of cellular and molecular changes in mammary epithelial cells (MECs) of female adults. In addition, pregnancy can also modify the predisposition of rodent and human MECs to initiate oncogenesis. Here, we investigate how pregnancy reprograms enhancer chromatin in the mammary epithelium of mice and influences the transcriptional output of the oncogenic transcription factor cMYC. We find that pregnancy induces an expansion of the active cis-regulatory landscape of MECs, which influences the activation of pregnancy-related programs during re-exposure to pregnancy hormones in vivo and in vitro. Using inducible cMYC overexpression, we demonstrate that post-pregnancy MECs are resistant to the downstream molecular programs induced by cMYC, a response that blunts carcinoma initiation, but does not perturb the normal pregnancy-induced epigenomic landscape. cMYC overexpression drives post-pregnancy MECs into a senescence-like state, and perturbations of this state increase malignant phenotypic changes. Taken together, our findings provide further insight into the cell-autonomous signals in post-pregnancy MECs that underpin the regulation of gene expression, cellular activation, and resistance to malignant development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.