ReviewCancers2021
Structural Chromosome Instability: Types, Origins, Consequences, and Therapeutic Opportunities.
Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Systemic Alterations of Cancer Cells and Their Boost by Polyploidization: Unicellular Attractor (UCA) Model.International journal of molecular sciences · 2023Pooled it
- Burst of aneuploidy: a cost of adaptation driven by breakdown of cell cycle control.Molecular systems biology · 2026Article
- Centromeric tandem repeats expansions in plateau zokor enhance chromosome stability for high-altitude adaptation.Genome biology · 2026Article
- Advances in Colorectal Cancer Cell Biology and Clonal Evolution.International journal of molecular sciences · 2026Review
- Article
- Wnt10b signaling regulates replication stress-induced chromosomal instability in human cancer.Life science alliance · 2025Article
- KDM4A serves as an α-tubulin demethylase regulating microtubule polymerization and cell mitosis.Science advances · 2025Article
- Endogenous p21 levels protect genomic stability by suppressing both excess and restrained nascent DNA syntheses.Science advances · 2025Article
- Integrated Assessment of Silver Nanoparticles on Plant Growth and Cytogenotoxicity UsingJournal of xenobiotics · 2025Article
- The SPINK Protein Family in Cancer: Emerging Roles in Tumor Progression, Therapeutic Resistance, and Precision Oncology.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Cyto-Genotoxic Assessment of Sulfoxaflor in Allium cepa Root Cells and DNA Docking Studies.Microscopy research and technique · 2025Article
- micronuclAI enables automated quantification of micronuclei for assessment of chromosomal instability.Communications biology · 2025Article
- Epigenomic Echoes-Decoding Genomic and Epigenetic Instability to Distinguish Lung Cancer Types and Predict Relapse.Epigenomes · 2025Review
- Chromothripsis in cancer.Nature reviews. Cancer · 2025Review
- The genetic architecture of bone metastases: unveiling the role of epigenetic and genetic modifications in drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- HSATII RNA-dependent triplex formation in early human embryogenesis as a potential mechanism for Y chromosome loss in Turner syndrome.Frontiers in molecular biosciences · 2025Article
- Article
- Signaling pathways involved in colorectal cancer: pathogenesis and targeted therapy.Signal transduction and targeted therapy · 2024Review
- Genetic and epigenetic instability as an underlying driver of progression and aggressive behavior in IDH-mutant astrocytoma.Acta neuropathologica · 2024Review
- Polyploidy in Cancer: Causal Mechanisms, Cancer-Specific Consequences, and Emerging Treatments.Molecular cancer therapeutics · 2024Review
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
Chromosomal instability (CIN) refers to an increased rate of acquisition of numerical and structural changes in chromosomes and is considered an enabling characteristic of tumors. Given its role as a facilitator of genomic changes, CIN is increasingly being considered as a possible therapeutic target, raising the question of which variables may convert CIN into an ally instead of an enemy during cancer treatment. This review discusses the origins of structural chromosome abnormalities and the cellular mechanisms that prevent and resolve them, as well as how different CIN phenotypes relate to each other. We discuss the possible fates of cells containing structural CIN, focusing on how a few cell duplication cycles suffice to induce profound CIN-mediated genome alterations. Because such alterations can promote tumor adaptation to treatment, we discuss currently proposed strategies to either avoid CIN or enhance CIN to a level that is no longer compatible with cell survival.
Indexed as
Identifiers
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.