ArticleCell cycle (Georgetown, Tex.)2018
DNA polymerase η mutational signatures are found in a variety of different types of cancer.
Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- Unraveling the lexicon of complex mutational phenomena in human cancers.Nature cancer · 2026Review
- Review
- Cellular and Molecular Mechanisms of Oxidative DNA Damage and Repair.Medicina (Kaunas, Lithuania) · 2025Review
- Endogenous p21 levels protect genomic stability by suppressing both excess and restrained nascent DNA syntheses.Science advances · 2025Article
- Widespread mutagenesis and chromosomal instability shape somatic genomes in systemic sclerosis.Nature communications · 2024Article
- Review
- Adaptive use of error-prone DNA polymerases provides flexibility in genome replication during tumorigenesis.Cancer science · 2024Review
- Meiotic DNA breaks drive multifaceted mutagenesis in the human germ line.Science (New York, N.Y.) · 2023Article
- Mutational signatures reveal mutual exclusivity of homologous recombination and mismatch repair deficiencies in colorectal and stomach tumors.Scientific data · 2023Article
- DNA damage response signaling: A common link between cancer and cardiovascular diseases.Cancer medicine · 2023Review
- Leveraging the replication stress response to optimize cancer therapy.Nature reviews. Cancer · 2023Review
- Spectrum of DNA mismatch repair failures viewed through the lens of cancer genomics and implications for therapy.Clinical science (London, England : 1979) · 2022Article
- Review
- Translesion polymerase eta both facilitates DNA replication and promotes increased human genetic variation at common fragile sites.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The origins and genetic interactions of KRAS mutations are allele- and tissue-specific.Nature communications · 2021Article
- Rad18 mediates specific mutational signatures and shapes the genomic landscape of carcinogen-induced tumorsNAR cancer · 2021Article
- DNA Methylation, Deamination, and Translesion Synthesis Combine to Generate Footprint Mutations in Cancer Driver Genes in B-Cell Derived Lymphomas and Other Cancers.Frontiers in genetics · 2021Article
- DNA mismatch repair promotes APOBEC3-mediated diffuse hypermutation in human cancers.Nature genetics · 2020Article
- DNA Damage: From Threat to Treatment.Cells · 2020Review
- Involvement of Rev1 in alkylating agent-induced loss of heterozygosity in Oryzias latipes.Genes to cells : devoted to molecular & cellular mechanisms · 2020Article
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Authors and funding
9 authors at 7 institutions in 3 countries.
Funding
Abstract
DNA polymerase (pol) η is a specialized error-prone polymerase with at least two quite different and contrasting cellular roles: to mitigate the genetic consequences of solar UV irradiation, and promote somatic hypermutation in the variable regions of immunoglobulin genes. Misregulation and mistargeting of pol η can compromise genome integrity. We explored whether the mutational signature of pol η could be found in datasets of human somatic mutations derived from normal and cancer cells. A substantial excess of single and tandem somatic mutations within known pol η mutable motifs was noted in skin cancer as well as in many other types of human cancer, suggesting that somatic mutations in A:T bases generated by DNA polymerase η are a common feature of tumorigenesis. Another peculiarity of pol ηmutational signatures, mutations in YCG motifs, led us to speculate that error-prone DNA synthesis opposite methylated CpG dinucleotides by misregulated pol η in tumors might constitute an additional mechanism of cytosine demethylation in this hypermutable dinucleotide.
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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.