Evidence map›Paper›PMID 26335399›Full record

ReviewRedox biology2015

The dual role of iNOS in cancer.

Federica Vannini, Khosrow Kashfi, Niharika Nath

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 265 papers.

0numbers the graph read from it
0cells of the map it votes in
265citing papers in PubMed
18.3field-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

265 citing papers in PubMed, 510 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Pro-tumor effects of nitric oxide from stress-upregulated inducible nitric oxide synthase in anti-tumor photodynamic therapy.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025
    Review
  12. Biological Activities and Phenolic Profile ofPlants (Basel, Switzerland) · 2025
    Article
  13. Article
  14. Programmed cell death in triple-negative breast cancer.Cellular & molecular biology letters · 2025
    Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

205 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

3 authors at 2 institutions in 1 country.

Federica VanniniDepartment of Physiology, Pharmacology and Neuroscience, Sophie Davis School of Biomedical Education, City University of New York Medical School, New York, NY 10031, United States.
Khosrow KashfiDepartment of Physiology, Pharmacology and Neuroscience, Sophie Davis School of Biomedical Education, City University of New York Medical School, New York, NY 10031, United States.
Niharika NathDepartment of Life Sciences, New York Institute of Technology, NY 10023, United States. Electronic address: nnath@nyit.edu.
City University of New York · USNew York Institute of Technology · US

Funding

MIDARP at CCNYR24DA018055 · NIDA · CITY COLLEGE OF NEW YORK · PI FRIEDMAN, EITAN · 2005 to 2010
$2.2M
NIDA NIH HHS R24DA018055
6 · The paper itself

Abstract

Nitric oxide (NO) is one of the 10 smallest molecules found in nature. It is a simple gaseous free radical whose predominant functions is that of a messenger through cGMP. In mammals, NO is synthesized by the enzyme nitric oxide synthase (NOS) of which there are three isoforms. Neuronal (nNOS, NOS1) and endothelial (eNOS, NOS3) are constitutive calcium-dependent forms of the enzyme that regulate neural and vascular function respectively. The third isoform (iNOS, NOS2), is calcium-independent and is inducible. In many tumors, iNOS expression is high, however, the role of iNOS during tumor development is very complex and quite perplexing, with both promoting and inhibiting actions having been described. This review will aim to summarize the dual actions of iNOS-derived NO showing that the microenvironment of the tumor is a contributing factor to these observations and ultimately to cellular outcomes.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntineoplastic AgentsBystander EffectCyclic GMPHumansHydroxymethylglutaryl-CoA Reductase InhibitorsNeoplasmsNF-kappa BNitric Oxide Synthase Type IIPolymorphism, GeneticSignal TransductionTumor MicroenvironmentAntineoplastic AgentsCyclic GMPHydroxymethylglutaryl-CoA Reductase InhibitorsNF-kappa BNitric Oxide Synthase Type IINOS2 protein, humanApoptosisCancerCell situationiNOSNitric oxideStroma

Identifiers

PMID26335399
PMCPMC4565017
OpenAlexW1148781016

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.