Evidence map›Paper›PMID 23901781›Full record

ReviewAntioxidants & redox signaling2014

Repair of oxidative DNA damage and cancer: recent progress in DNA base excision repair.

Timothy L Scott, Suganya Rangaswamy, Christina A Wicker, Tadahide Izumi

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

69 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  16. Zinc Ortho Methyl Carbonodithioate Improved Pre and Post-Synapse Memory Impairment via SIRT1/p-JNK Pathway against Scopolamine in Adult Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023
    Article
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  20. Review

9 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

4 authors.

Timothy L ScottGraduate Center for Toxicology, University of Kentucky , Lexington, Kentucky.
Suganya Rangaswamy
Christina A Wicker
Tadahide Izumi

Funding

Repair of oxidative DNA damage in mammalian cellsR01CA098664 · NCI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI IZUMI, TADAHIDE · 2003 to 2013
$2.4M
Repair of oxidative DNA damage in mammalian cellsR56CA098664 · NCI · LSU HEALTH SCIENCES CENTER · PI IZUMI, TADAHIDE · 2008 to 2008
$227k
NCI NIH HHS CA098664NCI NIH HHS CA098664-06S1
6 · The paper itself

Abstract

significanceReactive oxygen species (ROS) are generated by exogenous and environmental genotoxins, but also arise from mitochondria as byproducts of respiration in the body. ROS generate DNA damage of which pathological consequence, including cancer is well established. Research efforts are intense to understand the mechanism of DNA base excision repair, the primary mechanism to protect cells from genotoxicity caused by ROS. RECENT ADVANCES: In addition to the notion that oxidative DNA damage causes transformation of cells, recent studies have revealed how the mitochondrial deficiencies and ROS generation alter cell growth during the cancer transformation. CRITICAL ISSUES: The emphasis of this review is to highlight the importance of the cellular response to oxidative DNA damage during carcinogenesis. Oxidative DNA damage, including 7,8-dihydro-8-oxoguanine, play an important role during the cellular transformation. It is also becoming apparent that the unusual activity and subcellular distribution of apurinic/apyrimidinic endonuclease 1, an essential DNA repair factor/redox sensor, affect cancer malignancy by increasing cellular resistance to oxidative stress and by positively influencing cell proliferation. FUTURE DIRECTIONS: Technological advancement in cancer cell biology and genetics has enabled us to monitor the detailed DNA repair activities in the microenvironment. Precise understanding of the intracellular activities of DNA repair proteins for oxidative DNA damage should provide help in understanding how mitochondria, ROS, DNA damage, and repair influence cancer transformation.

Indexed as

DNA DamageDNA RepairAnimalsCell Transformation, NeoplasticDNA-(Apurinic or Apyrimidinic Site) LyaseHumansMitochondriaNeoplasmsOxidation-ReductionOxidative StressReactive Oxygen SpeciesAPEX1 protein, humanDNA-(Apurinic or Apyrimidinic Site) LyaseReactive Oxygen Species

Identifiers

PMID23901781
PMCPMC3960848

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.