Evidence map›Paper›PMID 23988267›Full record

ReviewCancer letters2014

Molecular mechanisms underlying chronic inflammation-associated cancers.

Yongzhong Wu, Smitha Antony, Jennifer L Meitzler, James H Doroshow

Open access · greenAbstract readReview
In one paragraph

Review in Cancer letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 2 pooled it
8.5field-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

156 citing papers in PubMed, 2 syntheses or guidelines pooled it, 294 citations in OpenAlex.

  1. Pooled it
  2. Association between TNF-α gene 308G>A polymorphism and lung cancer risk: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
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  5. Foods (Basel, Switzerland) · 2026
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96 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

4 authors at 2 institutions in 1 country.

Yongzhong WuLaboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Smitha AntonyLaboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Jennifer L MeitzlerLaboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
James H DoroshowLaboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA; Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: doroshoj@mail.nih.gov.
National Cancer Institute · USNational Institutes of Health · US

Funding

NADPH Oxidases as Novel Targets for Cancer TherapyZIABC010677 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DOROSHOW, JAMES · 2009 to 2025
$15.1M
Roles of NADPH Oxidase 5 and Dual Oxidase 2 in CancerZIABC011076 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DOROSHOW, JAMES · 2009 to 2016
$4.6M
Intramural NIH HHS ZIA BC010677Intramural NIH HHS ZIA BC011076
6 · The paper itself

Abstract

Although it is now accepted that chronic inflammation plays an essential role in tumorigenesis, the underlying molecular mechanisms linking inflammation and cancer remain to be fully explored. Inflammatory mediators present in the tumor microenvironment, including cytokines and growth factors, as well as reactive oxygen species (ROS) and reactive nitrogen species (RNS), have been implicated in the etiology of inflammation-associated cancers. Epithelial NADPH oxidase (Nox) family proteins, which generate ROS regulated by cytokines, are upregulated during chronic inflammation and cancer. ROS serve as effector molecules participating in host defense or as chemo-attractants recruiting leukocytes to wounds, thereby influencing the inflammatory reaction in damaged tissues. ROS can alter chromosomal DNA, leading to genomic instability, and may serve as signaling molecules that affect tumor cell proliferation, survival, metabolism, angiogenesis, and metastasis. Targeting Noxs and their downstream signaling components may be a promising approach to pre-empting inflammation-related malignancies.

Indexed as

AnimalsAnti-Inflammatory AgentsAntineoplastic AgentsCell Transformation, NeoplasticChronic DiseaseHumansInflammationInflammation MediatorsNADPH OxidasesNeoplasmsOxidative StressReactive Oxygen SpeciesSignal TransductionTranscription FactorsTumor MicroenvironmentAnti-Inflammatory AgentsAntineoplastic AgentsInflammation MediatorsNADPH OxidasesReactive Oxygen SpeciesTranscription FactorsCancerInflammationNADPH oxidaseReactive oxygen

Identifiers

PMID23988267
PMCPMC3935998
OpenAlexW2024328614

What OpenQuestion holds

Textmetadata
LicenceTDM
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.