ReviewCancer science2009
Chromosome segregation machinery and cancer.
Review in Cancer science, 2009. 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
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
30 citing papers in PubMed.
- TMEM106C, BSG, COPE, CDCA8, KPNA2, LIG1, UQCRH, and CCT5: Predictive of Survival and Immunotherapy Resistance in Hepatocellular Carcinoma.Human mutation · 2026Article
- Aberrant cohesin function in Saccharomyces cerevisiae activates Mcd1 degradation to promote cell lethality.PLoS genetics · 2025Article
- Human fibroblasts from aged individuals exhibit chromosomal instability through replication stress caused by oxidative stress.npj aging · 2025Article
- Aberrant cohesin function inbioRxiv : the preprint server for biology · 2025Article
- Dual role of lncRNA OTUD6B-AS1 in immune evasion and ferroptosis resistance: A prognostic and therapeutic biomarker in breast cancer.Non-coding RNA research · 2025Article
- HetFCM: functional co-module discovery by heterogeneous network co-clustering.Nucleic acids research · 2024Article
- Ethnic and racial-specific differences in levels of centrosome-associated mitotic kinases, proliferative and epithelial-to-mesenchymal markers in breast cancers.Cell division · 2022Article
- The ciliopathy protein CCDC66 controls mitotic progression and cytokinesis by promoting microtubule nucleation and organization.PLoS biology · 2022Article
- Chromatin Separation Regulators Predict the Prognosis and Immune Microenvironment Estimation in Lung Adenocarcinoma.Frontiers in genetics · 2022Article
- Attenuated Chromosome Oscillation as a Cause of Chromosomal Instability in Cancer Cells.Cancers · 2021Review
- SUMO-Targeted Ubiquitin Ligases and Their Functions in Maintaining Genome Stability.International journal of molecular sciences · 2021Review
- Automatic Detection Method for Cancer Cell Nucleus Image Based on Deep-Learning Analysis and Color Layer Signature Analysis Algorithm.Sensors (Basel, Switzerland) · 2020Article
- Centrosome aberrations and chromosome instability contribute to tumorigenesis and intra-tumor heterogeneity.Journal of cancer metastasis and treatment · 2018Article
- Kdm4c is Recruited to Mitotic Chromosomes and Is Relevant for Chromosomal Stability, Cell Migration and Invasion of Triple Negative Breast Cancer Cells.Breast cancer : basic and clinical research · 2018Article
- Review
- Essential role for centromeric factors following p53 loss and oncogenic transformation.Genes & development · 2017Article
- Targeted TPX2 increases chromosome missegregation and suppresses tumor cell growth in human prostate cancer.OncoTargets and therapy · 2017Article
- Achilles' heel of pluripotent stem cells: genetic, genomic and epigenetic variations during prolonged culture.Cellular and molecular life sciences : CMLS · 2016Review
- Antagonizing pathways leading to differential dynamics in colon carcinogenesis in Shugoshin1 (Sgo1)-haploinsufficient chromosome instability model.Molecular carcinogenesis · 2016Article
- KDM4C Activity Modulates Cell Proliferation and Chromosome Segregation in Triple-Negative Breast Cancer.Breast cancer : basic and clinical research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss or gain of chromosomes is associated with many cancer cells. This property, called chromosome instability, might arise from a lesion in the chromosome segregation machinery. Essential for chromosome segregation are the proper connection of microtubules to kinetochores, and the synchronous segregation of sister chromatids in anaphase. Accuracy of these processes is ensured by two sophisticated machineries called the correction mechanism and the spindle assembly checkpoint. Here we outline the current understanding of the underlying mechanisms, and highlight recent challenging experiments to address how chromosome segregation failure might relate to tumorigenesis. Understanding these mechanisms may lead to the discovery of new and improved anticancer therapies.
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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.