Evidence map›Paper›PMID 18978338›Full record

ReviewCarcinogenesis2009

Base excision repair of oxidative DNA damage and association with cancer and aging.

Scott Maynard, Shepherd H Schurman, Charlotte Harboe, Nadja C de Souza-Pinto, Vilhelm A Bohr

Open access · bronzeAbstract readReview
In one paragraph

Review in Carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 302 papers.

0numbers the graph read from it
0cells of the map it votes in
302citing papers in PubMed
14.9field-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

302 citing papers in PubMed, 668 citations in OpenAlex.

  1. Review
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  10. Genoprotective Properties ofInternational journal of molecular sciences · 2026
    Article
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  12. Review
  13. Review
  14. Review
  15. Frontiers in pharmacology · 2026
    Article
  16. Review
  17. Decoding the mechanism for cytotoxicity in thiolato-bridged triosmium carbonyl clusters: from serum reactivity to cellular impact.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2025
    Article
  18. Review
  19. Article
  20. Article

242 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.

Scott MaynardLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Shepherd H Schurman
Charlotte Harboe
Nadja C de Souza-Pinto
Vilhelm A Bohr
National Institute on Aging · USUniversidade de São Paulo · BR

Funding

DNA repair dysfunction in neurodegeneration and Alzheimer's DiseaseZIAAG000723 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$9.5M
Processing Of Oxidative Stress In AlzheimerZIAAG000735 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$9.4M
Mitochondrial DNA Repair Processes In Oxidative Stress And AgingZIAAG000733 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$9.2M
OXIDATIVE STRESS MITOCHONDRIAZ01AG000733 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1996 to 2008
$1.6M
REPAIR OF OXIDATIVE DNA DAMAGEZ01AG000727 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1994 to 2008
$1.3M
PROCESSING OF OXIDATIVE STRESS IN ALZHEIMER'S DISEASEZ01AG000735 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1997 to 2008
$565k
GROWTH ARREST AND DNA DAMAGE INDUCIBLE GENE GADD153--REGULATION BY DNA DAMAGEZ01AG000723 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM · 1992 to 2008
$310k
REGULATION OF GADD135 BY GROWTH ARREST, DIFFERENTIATION, AND METABOLIC STRESSESZ01AG000722 · NIA · AGING · PI HOLBROOK, N J · 1992 to 1993
–
Intramural NIH HHS
6 · The paper itself

Abstract

Aging has been associated with damage accumulation in the genome and with increased cancer incidence. Reactive oxygen species (ROS) are produced from endogenous sources, most notably the oxidative metabolism in the mitochondria, and from exogenous sources, such as ionizing radiation. ROS attack DNA readily, generating a variety of DNA lesions, such as oxidized bases and strand breaks. If not properly removed, DNA damage can be potentially devastating to normal cell physiology, leading to mutagenesis and/or cell death, especially in the case of cytotoxic lesions that block the progression of DNA/RNA polymerases. Damage-induced mutagenesis has been linked to various malignancies. The major mechanism that cells use to repair oxidative damage lesions, such as 8-hydroxyguanine, formamidopyrimidines, and 5-hydroxyuracil, is base excision repair (BER). The BER pathway in the nucleus is well elucidated. More recently, BER was shown to also exist in the mitochondria. Here, we review the association of BER of oxidative DNA damage with aging, cancer and other diseases.

Indexed as

Base PairingDNA DamageDNA RepairOxidative StressAgingAnimalsHumansNeoplasmsReactive Oxygen SpeciesSubcellular FractionsReactive Oxygen Species

Identifiers

PMID18978338
PMCPMC2639036
OpenAlexW2161085054

What OpenQuestion holds

Textmetadata
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.