ArticleOncogene2008
Aurora A overexpression induces cellular senescence in mammary gland hyperplastic tumors developed in p53-deficient mice.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 53 citations in OpenAlex.
- Tracking CDK1 Dynamics With a Novel Biosensor Mouse and Clinical Cohorts to Predict CDK4/6 Inhibitor Sensitivity in ER+ Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- LncTRDMT1-5 promotes chromosomal instability through MSRB3-mediated cell cycle and DNA damage in breast cancer.Frontiers in oncology · 2026Article
- Review
- The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024Review
- Aurora Kinase A proximity map reveals centriolar satellites as regulators of its ciliary function.EMBO reports · 2021Article
- Role of ARK5 in cancer and other diseases (Review).Experimental and therapeutic medicine · 2021Review
- Mechanisms of Oncogene-Induced Replication Stress: Jigsaw Falling into Place.Cancer discovery · 2018Review
- Aurora kinase-A overexpression in mouse mammary epithelium induces mammary adenocarcinomas harboring genetic alterations shared with human breast cancer.Carcinogenesis · 2016Article
- Functional Significance of Aurora Kinases-p53 Protein Family Interactions in Cancer.Frontiers in oncology · 2016Review
- TP53/p53 alterations and Aurora A expression in progressor and non-progressor colectomies from patients with longstanding ulcerative colitis.International journal of molecular medicine · 2015Article
- Scientific Rationale Supporting the Clinical Development Strategy for the Investigational Aurora A Kinase Inhibitor Alisertib in Cancer.Frontiers in oncology · 2015Review
- A growing role for Aurora A in chromosome instability.Nature cell biology · 2014Article
- Aurora-A: a potential DNA repair modulator.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Review
- Mitochondrial genome regulates mitotic fidelity by maintaining centrosomal homeostasis.Cell cycle (Georgetown, Tex.) · 2014Article
- The cancer biology of whole-chromosome instability.Oncogene · 2013Review
- Aurora kinase inhibitors: Potential molecular-targeted drugs for gynecologic malignant tumors.Biomedical reports · 2013Review
- Meta-analysis of Aurora Kinase A (AURKA) Expression Data Reveals a Significant Correlation Between Increased AURKA Expression and Distant Metastases in Human ER-positive Breast Cancers.Journal of data mining in genomics & proteomics · 2013Article
- Aurora A kinase (AURKA) in normal and pathological cell division.Cellular and molecular life sciences : CMLS · 2013Review
- Article
- Cellular senescence and tumor suppressor gene p16.International journal of cancer · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aurora A mitotic kinase is frequently overexpressed in various human cancers and is widely considered to be an oncoprotein. However, the cellular contexts in which Aurora A induces malignancy in vivo are still unclear. We previously reported a mouse model in which overexpression of human Aurora A in the mammary gland leads to small hyperplastic changes but not malignancy because of the induction of p53-dependent apoptosis. To study the additional factors required for Aurora A-associated tumorigenesis, we generated a new Aurora A overexpression mouse model that lacks p53. We present evidence here that Aurora A overexpression in primary mouse embryonic fibroblasts (MEFs) that lack p53 overrides postmitotic checkpoint and leads to the formation of multinucleated polyploid cells. Induction of Aurora A overexpression in the mammary glands of p53-deficient mice resulted in development of precancerous lesions that were histologically similar to atypical ductal hyperplasia in human mammary tissue and showed increased cellular senescence and p16 expression. We further observed DNA damage in p53-deficient primary MEFs after Aurora A overexpression. Our results suggest that Aurora A overexpression in mammary glands is insufficient for the development of malignant tumors in p53-deficient mice because of the induction of cellular senescence. Both p53 and p16 are critical in preventing mammary gland tumorigenesis in the Aurora A overexpression mouse model.
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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.