Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (625 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The products of chemical reactions that result in the addition of extraneous chemical groups to DNA.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: DNA Adduct; Adduct, DNA; Adducts, DNA.
Where it fits in the MeSH classification
- Broader topics
- DNA; DNA Damage
Research landscape
PubMed indexes 8,511 records tagged with the MeSH heading “DNA Adducts” (counts retrieved 2026-10-29). 587 of them (6.9%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 3,369 records.
Reviews account for 917 records (10.8%) and meta-analyses for 10. Randomized controlled trials number 36 (0.4%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,538 |
| 2000-2009 | 3,369 |
| 2010-2019 | 2,017 |
| 2020 onward | 587 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 917 | 10.8% |
| Meta-analyses | 10 | 0.1% |
| Randomized controlled trials | 36 | 0.4% |
Method: PubMed query "DNA Adducts"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in genetics and genomics
Genetic findings vary widely in strength. A variant linked to a condition in one study may not replicate in other ancestries, and most common variants have small effects that are meaningful only in aggregate. Studies of rare, high-impact variants can support strong causal claims about a gene, while association studies describe statistical links that need functional and independent replication. Check the sample size, the ancestry of participants, whether results were replicated, and whether a laboratory or clinical outcome was actually measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Differential damage and repair of DNA-adducts induced by anti-cancer drug cisplatin across mouse organs | 2019 | Research article Design not recorded in structured metadata | 184 | cc by PMID 30659176 · DOI · PMC6338751 |
| Polycyclic aromatic hydrocarbons and PAH-related DNA adducts | 2017 | Review article Design not recorded in structured metadata | 160 | cc by PMID 27943120 · DOI · PMC5509823 |
| PrimPol-dependent single-stranded gap formation mediates homologous recombination at bulky DNA adducts | 2020 | Research article Design not recorded in structured metadata | 110 | cc by PMID 33203852 · DOI · PMC7673990 |
| Semirandom DNA adducts regulate a filamentous defense-associated reverse transcriptase | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42271041 · DOI · PMC13275509 |
Differential damage and repair of DNA-adducts induced by anti-cancer drug cisplatin across mouse organs [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The platinum-based drug cisplatin is a widely used first-line therapy for several cancers.
- Closing excerpt
- Our approach should be applicable for studying drug resistance and for tailoring cancer chemotherapy regimens.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)
The platinum-based drug cisplatin is a widely used first-line therapy for several cancers. Cisplatin interacts with DNA mainly in the form of Pt-d(GpG) di-adduct, which stalls cell proliferation and activates DNA damage response. Although cisplatin shows a broad spectrum of anticancer activity, its utility is limited due to acquired drug resistance and toxicity to non-targeted tissues. Here, by integrating genome-wide high-throughput Damage-seq, XR-seq, and RNA-seq approaches, along with publicly available epigenomic data, we systematically study the genome-wide profiles of cisplatin damage formation and excision repair in mouse kidney, liver, lung and spleen. We find different DNA damage and repair spectra across mouse organs, which are associated with tissue-specific transcriptomic and epigenomic profiles. The framework and the multi-omics data we present here constitute an unbiased foundation for understanding the mechanisms of cellular response to cisplatin. Our approach should be applicable for studying drug resistance and for tailoring cancer chemotherapy regimens.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30659176 · DOI · PMC6338751
Polycyclic aromatic hydrocarbons and PAH-related DNA adducts [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Investigations on the impact of chemicals on the environment and human health have led to the development of an exposome concept.
- Closing excerpt
- Selected methods used for determination of DNA adducts have been presented.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (187 words)
Investigations on the impact of chemicals on the environment and human health have led to the development of an exposome concept. The exposome refers to the totality of exposures received by a person during life, including exposures to life-style factors, from the prenatal period to death. The exposure to genotoxic chemicals and their reactive metabolites can induce chemical modifications of DNA, such as, for example, DNA adducts, which have been extensively studied and which play a key role in chemically induced carcinogenesis. Development of different methods for the identification of DNA adducts has led to adopting DNA adductomic approaches. The ability to simultaneously detect multiple PAH-derived DNA adducts may allow for the improved assessment of exposure, and offer a mechanistic insight into the carcinogenic process following exposure to PAH mixtures. The major advantage of measuring chemical-specific DNA adducts is the assessment of a biologically effective dose. This review provides information about the occurrence of the polycyclic aromatic hydrocarbons (PAHs) and their influence on human exposure and biological effects, including PAH-derived DNA adduct formation and repair processes. Selected methods used for determination of DNA adducts have been presented.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27943120 · DOI · PMC5509823
PrimPol-dependent single-stranded gap formation mediates homologous recombination at bulky DNA adducts [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Stalled replication forks can be restarted and repaired by RAD51-mediated homologous recombination (HR), but HR can also perform post-replicative repair after bypass of the obstacle.
- Closing excerpt
- Our data support that HR at bulky adducts in mammalian cells involves post-replicative gap repair and define a role for PrimPol in HR-mediated DNA damage tolerance.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Stalled replication forks can be restarted and repaired by RAD51-mediated homologous recombination (HR), but HR can also perform post-replicative repair after bypass of the obstacle. Bulky DNA adducts are important replication-blocking lesions, but it is unknown whether they activate HR at stalled forks or behind ongoing forks. Using mainly BPDE-DNA adducts as model lesions, we show that HR induced by bulky adducts in mammalian cells predominantly occurs at post-replicative gaps formed by the DNA/RNA primase PrimPol. RAD51 recruitment under these conditions does not result from fork stalling, but rather occurs at gaps formed by PrimPol re-priming and resection by MRE11 and EXO1. In contrast, RAD51 loading at double-strand breaks does not require PrimPol. At bulky adducts, PrimPol promotes sister chromatid exchange and genetic recombination. Our data support that HR at bulky adducts in mammalian cells involves post-replicative gap repair and define a role for PrimPol in HR-mediated DNA damage tolerance.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33203852 · DOI · PMC7673990
Semirandom DNA adducts regulate a filamentous defense-associated reverse transcriptase [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Retrons and several defense-associated reverse transcriptases (DRTs) synthesize non-genomic DNA for bacteriophage immunity.
- Closing excerpt
- Functionally, DRT1 resembles a minimal retron where a single gene produces a reverse transcriptase, effector and non-genomic antitoxin DNA.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (139 words)
Retrons and several defense-associated reverse transcriptases (DRTs) synthesize non-genomic DNA for bacteriophage immunity. In some instances, this non-genomic DNA is of undefined, semirandom sequence. How undefined DNA sequences impart antiphage defense is not known. Herewe report the cryo-EM structure and functional characterization of the DRT1 antiphage defense system. We show that DRT1 performs template-free, protein-primed DNA synthesis to generate semirandom DNA adducts. DNA synthesis activates the nitrilase domain of DRT1, while DNA adducts drive the assembly of quiescent DRT1 filaments. Filamentous DRT1 is composed of domain-swapped C termini that are entwined, forming pseudoknots between tetrameric stacks. This configuration occludes conserved active-site residues, resulting in a dormant state. Bacteriophage escape mutants identify a T4 single-stranded DNA helicase required for DRT1 activity. Functionally, DRT1 resembles a minimal retron where a single gene produces a reverse transcriptase, effector and non-genomic antitoxin DNA.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42271041 · DOI · PMC13275509
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Metabolic activation of polycyclic and heterocyclic aromatic hydrocarbons and DNA damage: a review [5]
- Research article Carcinogenic polycyclic aromatic hydrocarbon-DNA adducts and mechanism of action [6]
- Research article Estrogens as endogenous genotoxic agents--DNA adducts and mutations [7]
- Research article Platinum-DNA adduct, nucleotide excision repair and platinum based anti-cancer chemotherapy [8]
- Research article Importance of chromium-DNA adducts in mutagenicity and toxicity of chromium(VI) [9]
- Research article DNA adducts from acetaldehyde: implications for alcohol-related carcinogenesis [10]
References
- Yimit A, Adebali O, Sancar A, Jiang Y. Differential damage and repair of DNA-adducts induced by anti-cancer drug cisplatin across mouse organs. . 2019. PMID 30659176 · DOI · PMC6338751
- Ewa B, Danuta MŠ. Polycyclic aromatic hydrocarbons and PAH-related DNA adducts. . 2017. PMID 27943120 · DOI · PMC5509823
- Piberger AL, Bowry A, Kelly RDW, Walker AK, González-Acosta D, Bailey LJ, et al.. PrimPol-dependent single-stranded gap formation mediates homologous recombination at bulky DNA adducts. . 2020. PMID 33203852 · DOI · PMC7673990
- Neville N, Johnson NV, Escobar EE, Chiang CH, Nreca A, Johnson SR, et al.. Semirandom DNA adducts regulate a filamentous defense-associated reverse transcriptase. . 2026. PMID 42271041 · DOI · PMC13275509
- Xue W, Warshawsky D. Metabolic activation of polycyclic and heterocyclic aromatic hydrocarbons and DNA damage: a review. Toxicol Appl Pharmacol. 2005. PMID 15963346 · DOI
- Baird WM, Hooven LA, Mahadevan B. Carcinogenic polycyclic aromatic hydrocarbon-DNA adducts and mechanism of action. Environ Mol Mutagen. 2005. PMID 15688365 · DOI
- Cavalieri E, Frenkel K, Liehr JG, Rogan E, Roy D. Estrogens as endogenous genotoxic agents--DNA adducts and mutations. J Natl Cancer Inst Monogr. 2000. PMID 10963621 · DOI
- Reed E. Platinum-DNA adduct, nucleotide excision repair and platinum based anti-cancer chemotherapy. Cancer Treat Rev. 1998. PMID 9861196 · DOI
- Zhitkovich A. Importance of chromium-DNA adducts in mutagenicity and toxicity of chromium(VI). Chem Res Toxicol. 2005. PMID 15651842 · DOI
- Brooks PJ, Theruvathu JA. DNA adducts from acetaldehyde: implications for alcohol-related carcinogenesis. Alcohol. 2005. PMID 16054980 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.