ReviewDevelopmental cell2016
Living in CIN: Mitotic Infidelity and Its Consequences for Tumor Promotion and Suppression.
Review in Developmental cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
99 citing papers in PubMed, 153 citations in OpenAlex.
- High-risk HPV E6 induces an aneuploidy-prone chromosome congression defect through destabilization of CENP-E.Journal of virology · 2026Article
- Towards a unified model of aneuploid karyotype dynamics.PLoS genetics · 2026Article
- Interaction of IRS2 with PLK1 protects cells from mitotic stress.Cell death & disease · 2026Article
- Human oncogenic herpesvirus latency proteins activate NEK2 to promote chromosomal instability and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Multifaceted role of primary cilia and ciliary proteins: A potential nexus for hedgehog signaling and prostate cancer.Biochimica et biophysica acta. Molecular basis of disease · 2026Review
- Biological clocks keep a watch on mitosis.Nature cell biology · 2026Review
- Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer.Cancer discovery · 2025Article
- The SPINK Protein Family in Cancer: Emerging Roles in Tumor Progression, Therapeutic Resistance, and Precision Oncology.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Linear ubiquitination of p31Cell & bioscience · 2025Article
- The histone H3.3 K27M mutation suppresses Ser31phosphorylation and mitotic fidelity, which can directly drive gliomagenesis.Current biology : CB · 2025Article
- Assessment of Chromosome Oscillations in Mammalian Cells by Live Cell Imaging.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Docetaxel response in BRCA1,p53-deficient mammary tumor cells is affected by Huntingtin and BAP1.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Mechanobiology of the nucleus during the G2-M transition.Nucleus (Austin, Tex.) · 2024Review
- Targeting YES1 Disrupts Mitotic Fidelity and Potentiates the Response to Taxanes in Triple-Negative Breast Cancer.Cancer research · 2024Article
- The yin and yang of chromosomal instability in prostate cancer.Nature reviews. Urology · 2024Review
- Arabidopsis AN3 and OLIGOCELLULA genes link telomere maintenance mechanisms with cell division and expansion control.Plant molecular biology · 2024Article
- A whale of a tale: whale cells evade the driving mechanism for hexavalent chromium-induced chromosome instability.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Kinesin-7 CENP-E in tumorigenesis: Chromosome instability, spindle assembly checkpoint, and applications.Frontiers in molecular biosciences · 2024Review
- Hexavalent Chromium Targets Securin to Drive Numerical Chromosome Instability in Human Lung Cells.International journal of molecular sciences · 2023Article
- Arabidopsis AN3 and OLIGOCELLULA genes link telomere maintenance mechanisms with cell division and expansion control.Research square · 2023Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Errors in chromosome segregation during mitosis have been recognized as a hallmark of tumor cells since the late 1800s, resulting in the long-standing hypothesis that mitotic abnormalities drive tumorigenesis. Recent work has shown that mitotic defects can promote tumors, suppress them, or do neither, depending on the rate of chromosome missegregation. Here we discuss the causes of chromosome missegregation, their effects on tumor initiation and progression, and the evidence that increasing the rate of chromosome missegregation may be an effective chemotherapeutic strategy.
Indexed as
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What OpenQuestion holds
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.