ArticleNature communications2018
Defective DNA damage repair leads to frequent catastrophic genomic events in murine and human tumors.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 54 papers.
What it found
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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.
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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
54 citing papers in PubMed, 89 citations in OpenAlex.
- Murine osteosarcoma recapitulates the driver landscape and genomic complexity of osteosarcoma evolution in humans.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic modifications in cancer drug resistance: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Novel driver gene MDC1 confers homologous recombination repair deficiency and genomic instability in chemoresistant relapsing ovarian cancer.Journal of translational medicine · 2026Article
- Extrachromosomal circular DNA: a potential clinical therapeutic target in malignant tumors.Cellular & molecular biology letters · 2026Review
- Chromoanagenesis in Osteosarcoma.Biomolecules · 2025Review
- Chromothripsis in cancer.Nature reviews. Cancer · 2025Review
- Spatio-temporal transcriptomics of chromothriptic SHH-medulloblastoma identifies multiple genetic clones that resist treatment and drive relapse.Nature communications · 2024Article
- Multi-omic and single-cell profiling of chromothriptic medulloblastoma reveals genomic and transcriptomic consequences of genome instability.Nature communications · 2024Article
- Chromothripsis: an emerging crossroad from aberrant mitosis to therapeutic opportunities.Journal of molecular cell biology · 2024Review
- Crosstalk between BER and NHEJ in XRCC4-Deficient Cells Depending on hTERT Overexpression.International journal of molecular sciences · 2024Article
- Non-homologous end joining shapes the genomic rearrangement landscape of chromothripsis from mitotic errors.Nature communications · 2024Article
- Chromothripsis is a novel biomarker for prognosis and differentiation diagnosis of pancreatic neuroendocrine neoplasms.MedComm · 2024Article
- Scrambling the genome in cancer: causes and consequences of complex chromosome rearrangements.Nature reviews. Genetics · 2024Review
- DNp73 enhances tumor progression and immune evasion in multiple myeloma by targeting the MYC and MYCN pathways.Frontiers in immunology · 2024Article
- Accurate identification of structural variations from cancer samples.Briefings in bioinformatics · 2023Article
- Pharmacological inhibition of BAP1 recruits HERC2 to competitively dissociate BRCA1-BARD1, suppresses DNA repair and sensitizes CRC to radiotherapy.Acta pharmaceutica Sinica. B · 2023Article
- Advancements in Focal Amplification Detection in Tumor/Liquid Biopsies and Emerging Clinical Applications.Genes · 2023Review
- 2-Hydroxy-3-methylanthraquinone inhibits homologous recombination repair in osteosarcoma through the MYC-CHK1-RAD51 axis.Molecular medicine (Cambridge, Mass.) · 2023Article
- Chromosomal Rearrangements and Chromothripsis: The Alternative End Generation Model.International journal of molecular sciences · 2023Review
- Pan-cancer analysis of chromothripsis-related gene expression patterns indicates an association with tumor immune and therapeutic agent responses.Frontiers in oncology · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
24 authors at 6 institutions in 3 countries.
Funding
Abstract
Chromothripsis and chromoanasynthesis are catastrophic events leading to clustered genomic rearrangements. Whole-genome sequencing revealed frequent complex genomic rearrangements (n = 16/26) in brain tumors developing in mice deficient for factors involved in homologous-recombination-repair or non-homologous-end-joining. Catastrophic events were tightly linked to Myc/Mycn amplification, with increased DNA damage and inefficient apoptotic response already observable at early postnatal stages. Inhibition of repair processes and comparison of the mouse tumors with human medulloblastomas (n = 68) and glioblastomas (n = 32) identified chromothripsis as associated with MYC/MYCN gains and with DNA repair deficiencies, pointing towards therapeutic opportunities to target DNA repair defects in tumors with complex genomic rearrangements.
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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.