Evidence map›Paper›PMID 20717533›Full record

ReviewInternational journal of molecular sciences2010

Nitric oxide: perspectives and emerging studies of a well known cytotoxin.

William A Paradise, Benjamin J Vesper, Ajay Goel, Joshua D Waltonen, Kenneth W Altman, G Kenneth Haines, James A Radosevich

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. A549 cells adapted to high nitric oxide show reduced surface CEACAM expression and altered adhesion and migration properties.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  11. Article
  12. Part I-mechanism of adaptation: high nitric oxide adapted A549 cells show enhanced DNA damage response and activation of antiapoptotic pathways.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  13. Part II-mechanism of adaptation: A549 cells adapt to high concentration of nitric oxide through bypass of cell cycle checkpoints.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  14. Review
  15. Article
  16. Article
  17. Part I. Molecular and cellular characterization of high nitric oxide-adapted human breast adenocarcinoma cell lines.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
  18. Article
  19. Review
  20. Nitric oxide short-circuits interleukin-12-mediated tumor regression.Cancer immunology, immunotherapy : CII · 2011
    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

7 authors at 6 institutions in 1 country.

William A ParadiseCenter for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago, Chicago, IL 60612, USA; E-Mails: paradise@uic.edu (W.A.P.); vesperbe@uic.edu (B.J.V.).
Benjamin J Vesper
Ajay Goel
Joshua D Waltonen
Kenneth W Altman
G Kenneth Haines
James A Radosevich
University of Illinois Chicago · USBaylor University Medical Center · USIcahn School of Medicine at Mount Sinai · USJesse Brown VA Medical Center · USWake Forest University · USYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The free radical nitric oxide (NO(*)) is known to play a dual role in human physiology and pathophysiology. At low levels, NO(*) can protect cells; however, at higher levels, NO(*) is a known cytotoxin, having been implicated in tumor angiogenesis and progression. While the majority of research devoted to understanding the role of NO(*) in cancer has to date been tissue-specific, we herein review underlying commonalities of NO(*) which may well exist among tumors arising from a variety of different sites. We also discuss the role of NO(*) in human physiology and pathophysiology, including the very important relationship between NO(*) and the glutathione-transferases, a class of protective enzymes involved in cellular protection. The emerging role of NO(*) in three main areas of epigenetics-DNA methylation, microRNAs, and histone modifications-is then discussed. Finally, we describe the recent development of a model cell line system in which human tumor cell lines were adapted to high NO(*) (HNO) levels. We anticipate that these HNO cell lines will serve as a useful tool in the ongoing efforts to better understand the role of NO(*) in cancer.

Indexed as

AnimalsCytotoxinsEpigenesis, GeneticGlutathione S-Transferase piHumansModels, BiologicalNeoplasmsNitric OxideReactive Nitrogen SpeciesCytotoxinsGlutathione S-Transferase piNitric OxideReactive Nitrogen Speciescytotoxicityepigeneticshigh NO adaptationnitric oxideoncogenetic

Identifiers

PMID20717533
PMCPMC2920563
OpenAlexW2086064799

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.