Evidence map›Paper›PMID 25417725›Full record

ArticleOncogenesis2014

Accumulation of abasic sites induces genomic instability in normal human gastric epithelial cells during Helicobacter pylori infection.

D Kidane, D L Murphy, J B Sweasy

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
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  10. Decoding mitochondrial DNA damage and repair associated withFrontiers in cellular and infection microbiology · 2024
    Review
  11. Article
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  20. Inhibition of EZH2 transactivation function sensitizes solid tumors to genotoxic stress.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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 1 institution in 1 country.

D KidaneDivision of Pharmacology and Toxicology, College of Pharmacy, Dell Pediatric Research Institute, The University of Texas at Austin, Austin, TX, USA.
D L MurphyDepartments of Therapeutic Radiology and Genetics, The Yale Comprehensive Cancer Center, New Haven, CT, USA.
J B SweasyDepartments of Therapeutic Radiology and Genetics, The Yale Comprehensive Cancer Center, New Haven, CT, USA.
The University of Texas at Austin · US

Funding

Characterization of a DNA Polymerase Beta Deficient MouseR01CA116753 · NCI · YALE UNIVERSITY · PI SWEASY, JOANN B. · 2006 to 2016
$2.8M
DNA Polymerase Beta and Gastric CancerK01CA154854 · NCI · YALE UNIVERSITY · PI KIDANE MULAT, DAWIT · 2011 to 2014
$318k
NCI NIH HHS K01 CA154854NCI NIH HHS R01 CA116753
6 · The paper itself

Abstract

Helicobacter pylori infection of the human stomach is associated with inflammation that leads to the release of reactive oxygen and nitrogen species (RONs), eliciting DNA damage in host cells. Unrepaired DNA damage leads to genomic instability that is associated with cancer. Base excision repair (BER) is critical to maintain genomic stability during RONs-induced DNA damage, but little is known about its role in processing DNA damage associated with H. pylori infection of normal gastric epithelial cells. Here, we show that upon H. pylori infection, abasic (AP) sites accumulate and lead to increased levels of double-stranded DNA breaks (DSBs). In contrast, downregulation of the OGG1 DNA glycosylase decreases the levels of both AP sites and DSBs during H. pylori infection. Processing of AP sites during different phases of the cell cycle leads to an elevation in the levels of DSBs. Therefore, the induction of oxidative DNA damage by H. pylori and subsequent processing by BER in normal gastric epithelial cells has the potential to lead to genomic instability that may have a role in the development of gastric cancer. Our results are consistent with the interpretation that precise coordination of BER processing of DNA damage is critical for the maintenance of genomic stability.

Identifiers

PMID25417725
PMCPMC4259965
OpenAlexW2050931542

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.