Evidence map›Paper›PMID 27494631›Full record

ReviewAntioxidants & redox signaling2017

Inducible Nitric Oxide Synthase in the Carcinogenesis of Gastrointestinal Cancers.

Graciele Almeida de Oliveira, Robert Y S Cheng, Lisa A Ridnour, Debashree Basudhar, Veena Somasundaram, Daniel W McVicar, Hugo Pequeno Monteiro, David A Wink

Open access · hybridAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
7.3field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 87 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. NO: a key player in microbiome dynamics and cancer pathogenesis.Frontiers in cellular and infection microbiology · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

8 authors at 2 institutions in 2 countries.

Graciele Almeida de Oliveira1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
Robert Y S Cheng1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
Lisa A Ridnour1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
Debashree Basudhar1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
Veena Somasundaram1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
Daniel W McVicar1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
Hugo Pequeno Monteiro2 Laboratório de Sinalização Celular, Universidade Federal de São Paulo , São Paulo, Brazil .
David A Wink1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
National Institutes of Health · USUniversidade Federal de São Paulo · BR

Funding

Nitric Oxide as a Modifier of Oxidative StressZIASC007281 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI WINK, DAVID · 2009 to 2025
$8.1M
6 · The paper itself

Abstract

significanceGastrointestinal (GI) cancer taken together constitutes one of the most common cancers worldwide with a broad range of etiological mechanisms. In this review, we have examined the impact of nitric oxide (NO) on the etiology of colon, colorectal, gastric, esophageal, and liver cancers. Recent Advances: Despite differences in etiology, initiation, and progression, chronic inflammation has been shown to be a common element within these cancers showing interactions of numerous pathways. NO generated at the inflammatory site contributes to the initiation and progression of disease. The amount of NO generated, time, and site vary and are an important determinant of the biological effects initiated. Among the nitric oxide synthase enzymes, the inducible isoform has the most diverse range, participating in numerous carcinogenic processes. There is emerging evidence showing that inducible nitric oxide synthase (NOS2) plays a central role in the process of tumor initiation and/or development. CRITICAL ISSUES: Redox inflammation through NOS2 and cyclooxygenase-2 participates in driving the mechanisms of initiation and progression in GI cancers. FUTURE DIRECTIONS: Understanding the underlying mechanism involved in NOS2 activation can provide new insights into important prevention and treatment strategies. Antioxid. Redox Signal. 26, 1059-1077.

Indexed as

AnimalsCarcinogenesisCyclooxygenase 2Disease ProgressionGastrointestinal NeoplasmsHumansInflammationNitric OxideNitric Oxide Synthase Type IIOxidation-ReductionCyclooxygenase 2Nitric OxideNitric Oxide Synthase Type IINOS2 protein, humanPTGS2 protein, humangastrointestinal cancerlivernitric oxide

Identifiers

PMID27494631
PMCPMC5488308
OpenAlexW2501946307

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.