Evidence map›Paper›PMID 18521188›Full record

ArticleThe Journal of clinical investigation2008

DNA damage induced by chronic inflammation contributes to colon carcinogenesis in mice.

Lisiane B Meira, James M Bugni, Stephanie L Green, Chung-Wei Lee, Bo Pang, Diana Borenshtein, Barry H Rickman, Arlin B Rogers, Catherine A Moroski-Erkul, Jose L McFaline and 4 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 307 papers.

0numbers the graph read from it
0cells of the map it votes in
307citing papers in PubMed
27.3field-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

307 citing papers in PubMed, 543 citations in OpenAlex.

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  15. Outer Membrane Vesicles FromJournal of extracellular biology · 2025
    Article
  16. Article
  17. The Link Between Human Alkyladenine DNA Glycosylase and Cancer Development.International journal of molecular sciences · 2025
    Review
  18. Article
  19. Review
  20. Article

247 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

14 authors at 1 institution in 1 country.

Lisiane B MeiraDepartment of Biological Engineering and Center for Environmental Health Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
James M Bugni
Stephanie L Green
Chung-Wei Lee
Bo Pang
Diana Borenshtein
Barry H Rickman
Arlin B Rogers
Catherine A Moroski-Erkul
Jose L McFaline
David B Schauer
Peter C Dedon
James G Fox
Leona D Samson
Massachusetts Institute of Technology · US

Funding

TOXICOLOGY CORE UNITP30ES002109 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LEVINE, STUART S · 1985 to 2020
$25.6M
IN VIVO ROLE OF DNA ALKYLATION REPAIRR01CA075576 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 1997 to 2011
$4.9M
IN VIVO PATHOGENESIS OF HELICOBACTER PYLORIR01AI037750 · NIAID · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI FOX, JAMES G · 1996 to 2009
$3.5M
NCI NIH HHS CA75576NCI NIH HHS R01 CA075576NIAID NIH HHS AI37750NIAID NIH HHS R01 AI037750NIEHS NIH HHS ES02109NIEHS NIH HHS P30 ES002109
6 · The paper itself

Abstract

Chronic inflammation increases cancer risk. While it is clear that cell signaling elicited by inflammatory cytokines promotes tumor development, the impact of DNA damage production resulting from inflammation-associated reactive oxygen and nitrogen species (RONS) on tumor development has not been directly tested. RONS induce DNA damage that can be recognized by alkyladenine DNA glycosylase (Aag) to initiate base excision repair. Using a mouse model of episodic inflammatory bowel disease by repeated administration of dextran sulfate sodium in the drinking water, we show that Aag-mediated DNA repair prevents colonic epithelial damage and reduces the severity of dextran sulfate sodium-induced colon tumorigenesis. Importantly, DNA base lesions expected to be induced by RONS and recognized by Aag accumulated to higher levels in Aag-deficient animals following stimulation of colonic inflammation. Finally, as a test of the generality of this effect we show that Aag-deficient animals display more severe gastric lesions that are precursors of gastric cancer after chronic infection with Helicobacter pylori. These data demonstrate that the repair of DNA lesions formed by RONS during chronic inflammation is important for protection against colon carcinogenesis.

Indexed as

DNA DamageAnimalsbeta CateninColonColonic NeoplasmsDextran SulfateDNA GlycosylasesDNA RepairHelicobacter InfectionsHelicobacter pyloriInflammatory Bowel DiseasesMaleMiceMice, Inbred C57BLMice, KnockoutModels, Biological3-methyladenine-DNA glycosylasebeta CateninCTNNB1 protein, mouseDextran SulfateDNA GlycosylasesHras protein, mouseProto-Oncogene Proteins p21(ras)PurinesPyrimidinesReactive Nitrogen SpeciesReactive Oxygen Species

Identifiers

PMID18521188
PMCPMC2423313
OpenAlexW2153724086

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.