Evidence map›Paper›PMID 12518062›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2003

Nitric oxide-induced cellular stress and p53 activation in chronic inflammation.

Lorne J Hofseth, Shin'ichi Saito, S Perwez Hussain, Michael G Espey, Katrina M Miranda, Yuzuru Araki, Chamelli Jhappan, Yuichiro Higashimoto, Peijun He, Steven P Linke and 6 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

115 citing papers in PubMed, 348 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Nitric Oxide Signaling and Sensing in Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Inflammatory bowel disease and carcinogenesis.Cancer metastasis reviews · 2022
    Review
  15. NOS2 andProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

55 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

16 authors at 3 institutions in 2 countries.

Lorne J HofsethLaboratories of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Shin'ichi Saito
S Perwez Hussain
Michael G Espey
Katrina M Miranda
Yuzuru Araki
Chamelli Jhappan
Yuichiro Higashimoto
Peijun He
Steven P Linke
Martha M Quezado
Irit Zurer
Varda Rotter
David A Wink
Ettore Appella
Curtis C Harris
Weizmann Institute of Science · ILNational Institutes of Health · USNational Cancer Institute · US

Funding

Inflammation and CancerZIABC010033 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 2009 to 2012
$2.9M
THE ROLE OF TOBACCO-RELATED CHEMICAL CARCINOGENS AND OXYRADICALS IN HUMAN CANCERZ01BC010033 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 1996 to 2008
$2.4M
6 · The paper itself

Abstract

Free radical-induced cellular stress contributes to cancer during chronic inflammation. Here, we investigated mechanisms of p53 activation by the free radical, NO. NO from donor drugs induced both ataxia-telangiectasia mutated (ATM)- and ataxia-telangiectasia mutated and Rad3-related-dependent p53 posttranslational modifications, leading to an increase in p53 transcriptional targets and a G(2)M cell cycle checkpoint. Such modifications were also identified in cells cocultured with NO-releasing macrophages. In noncancerous colon tissues from patients with ulcerative colitis (a cancer-prone chronic inflammatory disease), inducible NO synthase protein levels were positively correlated with p53 serine 15 phosphorylation levels. Immunostaining of HDM-2 and p21(WAF1) was consistent with transcriptionally active p53. Our study highlights a pivotal role of NO in the induction of cellular stress and the activation of a p53 response pathway during chronic inflammation.

Indexed as

DNA DamageAnimalsAtaxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsBreast NeoplasmsCell CycleCell Cycle ProteinsCell LineCoculture TechniquesColitis, UlcerativeComet AssayCyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsFemaleFree RadicalsAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCDKN1A protein, humanCdkn1a protein, mouseCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsFree RadicalsInterferon-gammaLipopolysaccharidesNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINOS2 protein, humanNos2 protein, mousePhosphoserineProtein Serine-Threonine KinasesTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID12518062
PMCPMC140909
OpenAlexW2101430535

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.