ArticleCommunications biology2020
Mutational signature SBS8 predominantly arises due to late replication errors in cancer.
Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 75 citations in OpenAlex.
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- Multi-omic analysis identifies a multi-step pathology in a case of multiple chorangioma syndrome in monochorionic twins.Orphanet journal of rare diseases · 2026Article
- The Mutational Epidemiology of Childhood Cancer.Clinical chemistry · 2025Review
- Investigation of DNA Damage Response Genes Validates the Role of DNA Repair in Pediatric Cancer Risk and IdentifiesJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025Article
- Single-cell analysis of the somatic mutational landscape in human chondrocytes during aging and in osteoarthritis.Nature aging · 2025Article
- Genomic landscape of endometrial polyps.Genome medicine · 2025Article
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- Unveiling Replication Timing-Dependent Mutational Biases: Mechanistic Insights from Gene Knockouts and Genotoxins Exposures.International journal of molecular sciences · 2025Article
- Uniquely high spontaneous mutational load in blood cells of XP-C patients.bioRxiv : the preprint server for biology · 2025Article
- Joint inference of mutational signatures from indels and single-nucleotide substitutions reveals prognostic impact of DNA repair deficiencies.Genome medicine · 2025Article
- Colibactin Exerts Androgen-dependent and -independent Effects on Prostate Cancer.European urology oncology · 2025Article
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- A review on trends in development and translation of omics signatures in cancer.Computational and structural biotechnology journal · 2024Review
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- Prevalence of germline variants in Brazilian pancreatic carcinoma patients.Scientific reports · 2024Article
- The mutagenic forces shaping the genomic landscape of lung cancer in never smokers.medRxiv : the preprint server for health sciences · 2024Article
- An ATR-PrimPol pathway confers tolerance to oncogenic KRAS-induced and heterochromatin-associated replication stress.Nature communications · 2023Article
- Genetic subdivisions of follicular lymphoma defined by distinct coding and noncoding mutation patterns.Blood · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Although a majority of somatic mutations in cancer are passengers, their mutational signatures provide mechanistic insights into mutagenesis and DNA repair processes. Mutational signature SBS8 is common in most cancers, but its etiology is debated. Incorporating genomic, epigenomic, and cellular process features for multiple cell-types we develop genome-wide composite epigenomic context-maps relevant for mutagenesis and DNA repair. Analyzing somatic mutation data from multiple cancer types in their epigenomic contexts, we show that SBS8 preferentially occurs in gene-poor, lamina-proximal, late replicating heterochromatin domains. While SBS8 is uncommon among mutations in non-malignant tissues, in tumor genomes its proportions increase with replication timing and speed, and checkpoint defects further promote this signature - suggesting that SBS8 probably arises due to uncorrected late replication errors during cancer progression. Our observations offer a potential reconciliation among different perspectives in the debate about the etiology of SBS8 and its relationship with other mutational signatures.
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