Evidence map›Paper›PMID 21387284›Full record

ReviewInternational journal of cancer2011

Reactive species and DNA damage in chronic inflammation: reconciling chemical mechanisms and biological fates.

Pallavi Lonkar, Peter C Dedon

Open access · bronzeAbstract readReview
In one paragraph

Review in International journal of cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
167citing papers in PubMed, 2 pooled it
0.6field-weighted citation impact, top 34% 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

167 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Oxidative Stress and DNA Damage at Telomeres.Cold Spring Harbor perspectives in biology · 2025
    Review
  17. Investigating DNA damage caused by COVID-19 and influenza in post COVID-19.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Article
  18. Article
  19. Review
  20. Review

107 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

2 authors at 2 institutions in 1 country.

Pallavi LonkarDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Peter C Dedon
In-Q-Tel · USMassachusetts Institute of Technology · US

Funding

TOXICOLOGY CORE UNITP30ES002109 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI YAFFE, MICHAEL B · 1985 to 2020
$25.6M
Reaction and Diffusion of NO in Biological SystemsP01CA026731 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI ESSIGMANN, JOHN M · 1985 to 2018
$25.4M
Chemistry and Biology of Deoxyribose Oxidation in DNAR01CA103146 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI DEDON, PETER C · 2003 to 2012
$3.8M
RNA Modifications as Biomarkers of Environmental Stress and InflammationR01ES017010 · NIEHS · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI BEGLEY, THOMAS J · 2009 to 2013
$2.1M
DNA Ocidation Products and Endogenous DNA AdductsR01ES016450 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI DEDON, PETER C · 2007 to 2011
$1.6M
Basis for sequence selective guanine oxidation in DNAR01CA110261 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI DEDON, PETER C · 2004 to 2008
$1.5M
Genetic toxicology of purine metabolismR01CA116318 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI DEDON, PETER C · 2006 to 2010
$1.3M
NCI NIH HHS CA026731NCI NIH HHS CA103146NCI NIH HHS CA116318NCI NIH HHS P01 CA026731NCI NIH HHS R01 CA103146NCI NIH HHS R01 CA110261NCI NIH HHS R01 CA116318NIEHS NIH HHS ES002109NIEHS NIH HHS ES016450NIEHS NIH HHS ES017010NIEHS NIH HHS P30 ES002109NIEHS NIH HHS R01 ES016450NIEHS NIH HHS R01 ES017010
6 · The paper itself

Abstract

Chronic inflammation has long been recognized as a risk factor for many human cancers. One mechanistic link between inflammation and cancer involves the generation of nitric oxide, superoxide and other reactive oxygen and nitrogen species by macrophages and neutrophils that infiltrate sites of inflammation. Although pathologically high levels of these reactive species cause damage to biological molecules, including DNA, nitric oxide at lower levels plays important physiological roles in cell signaling and apoptosis. This raises the question of inflammation-induced imbalances in physiological and pathological pathways mediated by chemical mediators of inflammation. At pathological levels, the damage sustained by nucleic acids represents the full spectrum of chemistries and likely plays an important role in carcinogenesis. This suggests that DNA damage products could serve as biomarkers of inflammation and oxidative stress in clinically accessible compartments such as blood and urine. However, recent studies of the biotransformation of DNA damage products before excretion point to a weakness in our understanding of the biological fates of the DNA lesions and thus to a limitation in the use of DNA lesions as biomarkers. This review will address these and other issues surrounding inflammation-mediated DNA damage on the road to cancer.

Indexed as

AnimalsCell Transformation, NeoplasticChronic DiseaseDNA DamageHumansInflammationNeoplasmsReactive Nitrogen SpeciesReactive Oxygen SpeciesRisk FactorsReactive Nitrogen SpeciesReactive Oxygen Species

Identifiers

PMID21387284
PMCPMC3334345
OpenAlexW1536009735

What OpenQuestion holds

Textmetadata
LicenceTDM
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.