ArticleCell reports2018
Identification of Drivers of Aneuploidy in Breast Tumors.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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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Who cites it
40 citing papers in PubMed, 63 citations in OpenAlex.
- Spindle Assembly Checkpoint Competency Determines Sensitivity to KIF18A Inhibition in Small Cell Lung Cancer.Cancer research communications · 2026Article
- Increased expression of a subset of genes within reduced copy number regions across multiple cancer types.bioRxiv : the preprint server for biology · 2026Article
- FOXM1 Signaling Network Transcriptionally Upregulates Expression of Proteins Involved in Mitotic Progression to Induce High Proliferation and Chromosomal Instability in Androgen Receptor-Low Triple-Negative Breast Cancer.International journal of molecular sciences · 2026Article
- Loss of negative regulation by HDAC1 and REST contributes to MAD1 overexpression in breast cancer.Molecular biology of the cell · 2025Article
- Targeting SUMOylation in ovarian cancer: Sensitivity, resistance, and the role of MYC.iScience · 2025Article
- Transcriptome Analysis of Canine Histiocytic Sarcoma Tumors and Cell Lines Reveals Multiple Targets for Therapy.Cancers · 2025Article
- Optimal strategies for correcting merotelic chromosome attachments in anaphase.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A new insight into the impact of copy number variations on cell cycle deregulation of luminal-type breast cancer.Oncology reviews · 2025Review
- Carcinogenesis trajectories.Frontiers in cell and developmental biology · 2025Article
- Cell Migration-Proliferation Dichotomy in Cancer: Biological Fact or Experimental Artefact?Biology · 2024Article
- Review
- Contribution of CENP-F to FOXM1-Mediated Discordant Centromere and Kinetochore Transcriptional Regulation.Molecular and cellular biology · 2024Article
- Double-checking chromosome segregation.The Journal of cell biology · 2023Review
- Harnessing transcriptionally driven chromosomal instability adaptation to target therapy-refractory lethal prostate cancer.Cell reports. Medicine · 2023Article
- Transcription factor E2F8 is a therapeutic target in the basal-like subtype of breast cancer.Frontiers in oncology · 2023Article
- Aurora kinases: Generators of spatial control during mitosis.Frontiers in cell and developmental biology · 2023Review
- Mesenchymal tumor cells drive adaptive resistance of Trp53Molecular oncology · 2022Article
- Knockdown of CKAP2 Inhibits Proliferation, Migration, and Aggregate Formation in Aggressive Breast Cancer.Cancers · 2022Article
- Tip60 acetylation of histone H3K4 temporally controls chromosome passenger complex localization.Molecular biology of the cell · 2022Article
- Effects of aneuploidy on cell behaviour and function.Nature reviews. Molecular cell biology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Although aneuploidy is found in the majority of tumors, the degree of aneuploidy varies widely. It is unclear how cancer cells become aneuploid or how highly aneuploid tumors are different from those of more normal ploidy. We developed a simple computational method that measures the degree of aneuploidy or structural rearrangements of large chromosome regions of 522 human breast tumors from The Cancer Genome Atlas (TCGA). Highly aneuploid tumors overexpress activators of mitotic transcription and the genes encoding proteins that segregate chromosomes. Overexpression of three mitotic transcriptional regulators, E2F1, MYBL2, and FOXM1, is sufficient to increase the rate of lagging anaphase chromosomes in a non-transformed vertebrate tissue, demonstrating that this event can initiate aneuploidy. Highly aneuploid human breast tumors are also enriched in TP53 mutations. TP53 mutations co-associate with the overexpression of mitotic transcriptional activators, suggesting that these events work together to provide fitness to breast tumors.
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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.