ArticleScientific reports2022
Echoed induction of nucleotide variants and chromosomal structural variants in cancer cells.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 5 citations in OpenAlex.
- Ionizing Radiation and Ultraviolet Light Irradiation-Associated DNA Damage Increasing Genomic Instability Risk.Cancer science · 2026Review
- Genome instability is increased during DNA replication in the presence of the CPD UV photoproduct in transcriptionally active genes.iScience · 2026Article
- Activation of Wnt/β-catenin signaling is critical for the tumorigenesis of choroid plexus.Neuro-oncology · 2025Article
- A genomic instability-associated lncRNA signature for predicting prognosis and biomarkers in lung adenocarcinoma.Scientific reports · 2024Article
- The clock-like accumulation of germline and somatic mutations can arise from the interplay of DNA damage and repair.PLoS biology · 2024Article
- Article
- Disentangling sources of clock-like mutations in germline and soma.bioRxiv : the preprint server for biology · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
Generally, the number of single-nucleotide variants (SNVs) in somatic cells increases with age, which is expected for replication errors. The number of SNVs in cancer cells, however, is often much higher than that in somatic cells, raising the question of whether cancer cells possess SNV induction pathways. The present study shows that the number of SNVs in cancer cells correlates with the number of chromosomal structural variants (SVs). While Kataegis, localized hypermutations typically arising near SV sites, revealed multiple SNVs within 1 kb, SV-associated SNVs were generally observed within 0.1-1 Mb of SV sites, irrespective of Kataegis status. SNVs enriched within 1 Mb of SV regions were associated with deficiency of DNA damage repair, including HR deficiency-associated single base substitution 3 (SBS3) and exogenous damage-associated SBS7 and SBS36 signatures. We also observed a similar correlation between SVs and SNVs in cells that had undergone clonal evolution in association with genomic instability, implying an association between genomic instability and SV-associated induction of SNVs.
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