ReviewSeminars in cell & developmental biology2022
Mechanistic origins of diverse genome rearrangements in cancer.
Review in Seminars in cell & developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Tumor evolution: signaling pathways, molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Acute Myeloid Leukemia with MYC Amplification on a Ring Chromosome 8.Internal medicine (Tokyo, Japan) · 2025Article
- Chromoplexy: A Pathway to Genomic Complexity and Cancer Development.International journal of molecular sciences · 2025Review
- Cell-cycle dependent DNA repair and replication unifies patterns of chromosome instability.Nature communications · 2025Article
- FuSViz-visualization and interpretation of structural variation using cancer genomics and transcriptomics data.Nucleic acids research · 2025Article
- Chromoplexy.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Diverse Genome Structures among Eukaryotes May Have Arisen in Response to Genetic Conflict.Genome biology and evolution · 2024Review
- Aneuploidy and complex genomic rearrangements in cancer evolution.Nature cancer · 2024Review
- DNA polymerases in precise and predictable CRISPR/Cas9-mediated chromosomal rearrangements.BMC biology · 2023Article
- Cell cycle responses to Topoisomerase II inhibition: Molecular mechanisms and clinical implications.The Journal of cell biology · 2023Review
- Flexible Attachment and Detachment of Centromeres and Telomeres to and from Chromosomes.Biomolecules · 2023Review
- The 3D genome and its impacts on human health and disease.Life medicine · 2023Review
- The Association of R-Loop Binding Proteins Subtypes with CIN Implicates Therapeutic Strategies in Colorectal Cancer.Cancers · 2022Article
- Phosphorylation of XPD drives its mitotic role independently of its DNA repair and transcription functions.Science advances · 2022Article
- Unravelling the tumour genome: The evolutionary and clinical impacts of structural variants in tumourigenesis.The Journal of pathology · 2022Review
- Translin facilitates RNA polymerase II dissociation and suppresses genome instability during RNase H2- and Dicer-deficiency.PLoS genetics · 2022Article
- CRISPR-based genome editing through the lens of DNA repair.Molecular cell · 2022Review
- KAT5 histone acetyltransferase mutations in cancer cells.microPublication biology · 2022Article
- Nuclear Envelope Integrity in Health and Disease: Consequences on Genome Instability and Inflammation.International journal of molecular sciences · 2021Review
- Distribution of copy number variations and rearrangement endpoints in human cancers with a review of literature.Mutation researchReview
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
Cancer genomes frequently harbor structural chromosomal rearrangements that disrupt the linear DNA sequence order and copy number. To date, diverse classes of structural variants have been identified across multiple cancer types. These aberrations span a wide spectrum of complexity, ranging from simple translocations to intricate patterns of rearrangements involving multiple chromosomes. Although most somatic rearrangements are acquired gradually throughout tumorigenesis, recent interrogation of cancer genomes have uncovered novel categories of complex rearrangements that arises rapidly through a one-off catastrophic event, including chromothripsis and chromoplexy. Here we review the cellular and molecular mechanisms contributing to the formation of diverse structural rearrangement classes during cancer development. Genotoxic stress from a myriad of extrinsic and intrinsic sources can trigger DNA double-strand breaks that are subjected to DNA repair with potentially mutagenic outcomes. We also highlight how aberrant nuclear structures generated through mitotic cell division errors, such as rupture-prone micronuclei and chromosome bridges, can instigate massive DNA damage and the formation of complex rearrangements in cancer genomes.
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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.