ArticleProceedings of the National Academy of Sciences of the United States of America2004
Estrogen mediates Aurora-A overexpression, centrosome amplification, chromosomal instability, and breast cancer in female ACI rats.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 135 citations in OpenAlex.
- R-loop editing by DNA cytosine deaminase APOBEC3B modulates the activity of oestrogen receptor enhancers.Nature communications · 2026Article
- Rat Models of Hormone Receptor-Positive Breast Cancer.Journal of mammary gland biology and neoplasia · 2024Review
- Article
- Stress keratin 17 and estrogen support viral persistence and modulate the immune environment during cervicovaginal murine papillomavirus infection.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- GPER1 links estrogens to centrosome amplification and chromosomal instability in human colon cells.Life science alliance · 2023Article
- The Anaphase-Promoting Complex/Cyclosome Is a Cellular Ageing Regulator.International journal of molecular sciences · 2022Review
- Review
- Induced mammary cancer in rat models: pathogenesis, genetics, and relevance to female breast cancer.Journal of mammary gland biology and neoplasia · 2022Review
- Review
- Centrosome Aberrations as Drivers of Chromosomal Instability in Breast Cancer.Endocrinology · 2021Review
- Mitotic kinases as drivers of the epithelial-to-mesenchymal transition and as therapeutic targets against breast cancers.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Dysregulation of the centrosome induced by BRCA1 deficiency contributes to tissue-specific carcinogenesis.Cancer science · 2021Review
- OTUD6A Is an Aurora Kinase A-Specific Deubiquitinase.International journal of molecular sciences · 2021Article
- Review
- Bioinformatics analysis identifies hub genes and pathways in nasopharyngeal carcinoma.Oncology letters · 2019Article
- Overcome cancer drug resistance by targeting epigenetic modifications of centrosome.Cancer drug resistance (Alhambra, Calif.) · 2019Review
- Modeling Human Ductal Carcinoma In Situ in the Mouse.Journal of mammary gland biology and neoplasia · 2018Review
- Rat models of 17β-estradiol-induced mammary cancer reveal novel insights into breast cancer etiology and prevention.Physiological genomics · 2018Review
- Centriole Overduplication is the Predominant Mechanism Leading to Centrosome Amplification in Melanoma.Molecular cancer research : MCR · 2018Article
- Centrosome amplification: a suspect in breast cancer and racial disparities.Endocrine-related cancer · 2017Review
12 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Estrogens play a crucial role in the causation and development of sporadic human breast cancer (BC). Chromosomal instability (CIN) is a defining trait of early human ductal carcinoma in situ (DCIS) and is believed to precipitate breast oncogenesis. We reported earlier that 100% of female ACI (August/Copenhagen/Irish) rats treated with essentially physiological serum levels of 17beta-estradiol lead to mammary gland tumors with histopathologic, cellular, molecular, and ploidy changes remarkably similar to those seen in human DCIS and invasive sporadic ductal BC. Aurora-A (Aur-A), a centrosome kinase, and centrosome amplification have been implicated in the origin of aneuploidy via CIN. After 4 mo of estradiol treatment, levels of Aur-A and centrosomal proteins, gamma-tubulin and centrin, rose significantly in female ACI rat mammary glands and remained elevated in mammary tumors at 5-6 mo of estrogen treatment. Centrosome amplification was initially detected at 3 mo of treatment in focal dysplasias, before DCIS. At 5-6 mo, 90% of the mammary tumor centrosomes were amplified. Comparative genomic hybridization revealed nonrandom amplified chromosome regions in seven chromosomes with a frequency of 55-82% in 11 primary tumors each from individual rats. Thus, we report that estrogen is causally linked via estrogen receptor alpha to Aur-A overexpression, centrosome amplification, CIN, and aneuploidy leading to BC in susceptible mammary gland cells.
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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.