Evidence map›Paper›PMID 30287511›Full record

ReviewBiochemical Society transactions2018

Carcinogens and DNA damage.

Jessica L Barnes, Maria Zubair, Kaarthik John, Miriam C Poirier, Francis L Martin

Open access · bronzeAbstract readReview
In one paragraph

Review in Biochemical Society transactions, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed, 2 pooled it
19.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

3 · Its place in the literature

Who cites it

129 citing papers in PubMed, 2 syntheses or guidelines pooled it, 309 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Oxidative stress in neurodegeneration: from a simple insult to a dynamic regulator.Redox report : communications in free radical research · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Tissue-Specific Prevalence and Clonal Architecture ofbioRxiv : the preprint server for biology · 2026
    Article
  11. Review
  12. Article
  13. Review
  14. Development of a DNA damage assay system using stable human hepatocytes.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2026
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Hypoxic adaptation theory of cancer.Frontiers in cell and developmental biology · 2026
    Article

69 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Jessica L BarnesSchool of Pharmacy and Biomedical Sciences, University of Central Lancashire, Preston PR1 2HE, U.K.
Maria ZubairSchool of Pharmacy and Biomedical Sciences, University of Central Lancashire, Preston PR1 2HE, U.K.
Kaarthik JohnCarcinogen-DNA Interactions Section, LCBG, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892-4255, U.S.A.
Miriam C PoirierCarcinogen-DNA Interactions Section, LCBG, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892-4255, U.S.A. flmartin@uclan.ac.uk miriam.poirier@nih.gov.
Francis L MartinSchool of Pharmacy and Biomedical Sciences, University of Central Lancashire, Preston PR1 2HE, U.K. flmartin@uclan.ac.uk miriam.poirier@nih.gov.
University of Lancashire · GBNational Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Humans are variously and continuously exposed to a wide range of different DNA-damaging agents, some of which are classed as carcinogens. DNA damage can arise from exposure to exogenous agents, but damage from endogenous processes is probably far more prevalent. That said, epidemiological studies of migrant populations from regions of low cancer risk to high cancer risk countries point to a role for environmental and/or lifestyle factors playing a pivotal part in cancer aetiology. One might reasonably surmise from this that carcinogens found in our environment or diet are culpable. Exposure to carcinogens is associated with various forms of DNA damage such as single-stand breaks, double-strand breaks, covalently bound chemical DNA adducts, oxidative-induced lesions and DNA-DNA or DNA-protein cross-links. This review predominantly concentrates on DNA damage induced by the following carcinogens: polycyclic aromatic hydrocarbons, heterocyclic aromatic amines, mycotoxins, ultraviolet light, ionising radiation, aristolochic acid, nitrosamines and particulate matter. Additionally, we allude to some of the cancer types where there is molecular epidemiological evidence that these agents are aetiological risk factors. The complex role that carcinogens play in the pathophysiology of cancer development remains obscure, but DNA damage remains pivotal to this process.

Indexed as

DNA DamageAminesAnimalsAristolochic AcidsBenzo(a)pyreneCarcinogensCross-Linking ReagentsDietDNADNA RepairFemaleHumansInflammationLung NeoplasmsMaleNeoplasmsAminesaristolochic acid IAristolochic AcidsBenzo(a)pyreneCarcinogensCross-Linking ReagentsDNAPolycyclic Aromatic HydrocarbonsbioactivationcancercarcinogensDNA damage

Identifiers

PMID30287511
PMCPMC6195640
OpenAlexW2894930578

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.