ReviewOncogene2013
The cancer biology of whole-chromosome instability.
Review in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.
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
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.
- No association between HMGB1 polymorphisms and cancer risk: evidence from a meta-analysis.Bioscience reports · 2018Pooled it
- Chromosomal Heterogeneity and Enrichment of Mitotic Regulatory Programs Reveal a Therapeutic Vulnerability in Cytarabine-Resistant FLT3-ITD AML.Current issues in molecular biology · 2026Article
- Deficiency in POLE Exonuclease Causes Synthetic Lethality in Highly Aneuploid Cancer Cells.Cancer research · 2026Article
- Etiology of polyploid giant cancer cells: a new frontier in cancer biology.Cancer cell international · 2026Review
- Oncotransformation in Bhas 42 Cell Transformation Assay by Typical Non-Genotoxic Carcinogens, PFOA and PFOS, and Time-Course Transcriptome Analysis.Biomolecules · 2025Article
- Elucidating the genotoxicity of Fusobacterium nucleatum-secreted mutagens in colorectal cancer carcinogenesis.Gut pathogens · 2024Article
- Patterns of Aneuploidy and Signaling Consequences in Cancer.Cancer research · 2024Review
- Impairment of α-tubulin and F-actin interactions of GJB3 induces aneuploidy in urothelial cells and promotes bladder cancer cell invasion.Cellular & molecular biology letters · 2024Article
- METTL16-mediated N6-methyladenosine modification of Soga1 enables proper chromosome segregation and chromosomal stability in colorectal cancer.Cell proliferation · 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
- The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability.Journal of experimental & clinical cancer research : CR · 2024Article
- Article
- Loss of ORP3 induces aneuploidy and promotes bladder cancer cell invasion through deregulated microtubule and actin dynamics.Cellular and molecular life sciences : CMLS · 2023Article
- Proliferative advantage of specific aneuploid cells drives evolution of tumor karyotypes.Biophysical journal · 2023Article
- Profiling chromosomal-level variations in gastric malignancies.Cancer science · 2022Article
- Reduced sister chromatid cohesion acts as a tumor penetrance modifier.PLoS genetics · 2022Article
- Endomembranes promote chromosome missegregation by ensheathing misaligned chromosomes.The Journal of cell biology · 2022Article
- Prognostic Implications and Immune Infiltration Characteristics of Chromosomal Instability-Related Dysregulated CeRNA in Lung Adenocarcinoma.Frontiers in molecular biosciences · 2022Article
- Clonal selection of stable aneuploidies in progenitor cells drives high-prevalence tumorigenesis.Genes & development · 2021Article
- Solving the chromosome puzzle of aneuploidy in cancer.Genes & development · 2021Review
19 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One form of chromosome instability (CIN), the recurrent missegregation of whole chromosomes during cell division (W-CIN), leads to aneuploidy. Although W-CIN is a hallmark of most cancers, mutations in genes involved in chromosome segregation are exceedingly rare. We discuss an oncogene-induced mitotic stress model that provides a mechanistic framework to explain this paradox. We also review the tumor-promoting and tumor-suppressing consequences of W-CIN. Importantly, we do this in the context of cancer as a complex systemic disease, rather than as a simple linearly progressing disorder that arises from a single abnormal cell population. Accordingly, we highlight the often neglected effects of W-CIN on key non-cell-autonomous entities, such as the immune system and the tumor microenvironment. Distinct tissue-specific susceptibilities to W-CIN-induced tumorigenesis and the clinical implications of W-CIN are also discussed.
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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.