Evidence map›Paper›PMID 20955798›Full record

ReviewSeminars in cancer biology2010

Variant base excision repair proteins: contributors to genomic instability.

Antonia A Nemec, Susan S Wallace, Joann B Sweasy

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

41 citing papers in PubMed, 72 citations in OpenAlex.

  1. The Link Between Human Alkyladenine DNA Glycosylase and Cancer Development.International journal of molecular sciences · 2025
    Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Neural Tube Defects and Folate Deficiency: Is DNA Repair Defective?International journal of molecular sciences · 2023
    Review
  7. Association ofFrontiers in genetics · 2022
    Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

3 authors at 2 institutions in 1 country.

Antonia A NemecDepartment of Therapeutic Radiology, 15 York Street, New Haven, CT 06510, United States.
Susan S Wallace
Joann B Sweasy
University of New Haven · USUniversity of Vermont · US

Funding

SUBSTRATE SPECIFICITY OF THE BER OXIDATIVE DNA GLYCOSYLASESP01CA098993 · NCI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI LEE, ANDREA J · 2004 to 2021
$25.9M
TUMOR SELECTIVE INACTIVATION OF THE REPAIR PROTEIN AGTP01CA129186 · NCI · YALE UNIVERSITY · PI SARTORELLI, ALAN CLAYTON · 2007 to 2012
$8.5M
Chemistry and Biology of Oxidized Purine Lesions in DNAR01CA090689 · NCI · UNIVERSITY OF UTAH · PI BURROWS, CYNTHIA J, DAVID, SHEILA SUE · 2002 to 2019
$5.5M
RESEARCH TRAINING: RADIATION THERAPY, BIOLOGY, PHYSICST32CA009259 · NCI · YALE UNIVERSITY · PI GLAZER, PETER M · 1985 to 2009
$1.4M
NCI NIH HHS CA129186NCI NIH HHS P01 CA090689NCI NIH HHS P01 CA098993NCI NIH HHS P01 CA129186NCI NIH HHS R01 CA090689NCI NIH HHS T32 CA009259
6 · The paper itself

Abstract

Cells sustain endogenous DNA damage at rates greater than 20,000 DNA lesions per cell per day. These damages occur largely as a result of the inherently unstable nature of DNA and the presence of reactive oxygen species within cells. The base excision repair system removes the majority of DNA lesions resulting from endogenous DNA damage. There are several enzymes that function during base excision repair. Importantly, there are over 100 germline single nucleotide polymorphisms in genes that function in base excision repair and that result in non-synonymous amino acid substitutions in the proteins they encode. Somatic variants of these enzymes are also found in human tumors. Variant repair enzymes catalyze aberrant base excision repair. Aberrant base excision repair combined with continuous endogenous DNA damage over time has the potential to lead to a mutator phenotype. Mutations that arise in key growth control genes, imbalances in chromosome number, chromosomal translocations, and loss of heterozygosity can result in the initiation of human cancer or its progression.

Indexed as

DNA RepairGenomic InstabilityMutationAmino Acid SubstitutionAnimalsChromosome AberrationsDNA-(Apurinic or Apyrimidinic Site) LyaseDNA-Binding ProteinsDNA DamageDNA-Directed DNA PolymeraseDNA GlycosylasesDNA Ligase ATPDNA LigasesDNA Repair EnzymesGene ExpressionHumansAPEX1 protein, humanDNA-(Apurinic or Apyrimidinic Site) LyaseDNA-Binding ProteinsDNA-Directed DNA PolymeraseDNA GlycosylasesDNA Ligase ATPDNA ligase III alpha protein, XenopusDNA LigasesDNA Repair EnzymesPoly-ADP-Ribose Binding ProteinsXenopus ProteinsX-ray Repair Cross Complementing Protein 1

Identifiers

PMID20955798
PMCPMC3254599
OpenAlexW2070335845

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.