Evidence map›Paper›PMID 23868870›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2013

Molecular pathways: inflammation-associated nitric-oxide production as a cancer-supporting redox mechanism and a potential therapeutic target.

Elizabeth A Grimm, Andrew G Sikora, Suhendan Ekmekcioglu

Abstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

58 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. All-Flex Plasma Patch for In Vivo Delivery of Reactive Species.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  6. Review
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  13. The Hydrophobic Extract ofMolecules (Basel, Switzerland) · 2023
    Article
  14. Article
  15. Effect of intermittency factor on singlet oxygen and PGEBiochemistry and biophysics reports · 2022
    Article
  16. Article
  17. Observational
  18. Article
  19. Review
  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

3 authors.

Elizabeth A GrimmAuthors' Affiliations: Department of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas; and Departments of Otolaryngology, Immunology, Oncological Science, and Dermatology, Mount Sinai School of Medicine, New York, New York.
Andrew G Sikora
Suhendan Ekmekcioglu

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
UT M.D. Anderson Cancer Center SPORE in MelanomaP50CA093459 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI GRIMM, ELIZABETH A · 2004 to 2014
$23.7M
TARGETING INOS TO INHIBIT MYELOID-DERIVED SUPPRESSOR CELLS (MDSC) IN MELANOMAK08CA154963 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI SIKORA, ANDREW · 2011 to 2015
$674k
Role of Activated EGFR and COX-2 in Metastasis and Escape from Tumor DormancyR03DE021741 · NIDCR · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI SIKORA, ANDREW · 2011 to 2012
$254k
NCI NIH HHS 1K08CA154963-01A1NCI NIH HHS K08 CA154963NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA093459NIDCR NIH HHS 5R03DE021741-02NIDCR NIH HHS R03 DE021741
6 · The paper itself

Abstract

It is widely accepted that many cancers express features of inflammation, driven by both microenvironmental cells and factors, and the intrinsic production of inflammation-associated mediators from malignant cells themselves. Inflammation results in intracellular oxidative stress with the ultimate biochemical oxidants composed of reactive nitrogens and oxygens. Although the role of inflammation in carcinogensis is well accepted, we now present data showing that inflammatory processes are also active in the maintenance phase of many aggressive forms of cancer. The oxidative stress of inflammation is proposed to drive a continuous process of DNA adducts and crosslinks, as well as posttranslational modifications to lipids and proteins that we argue support growth and survival. In this perspective, we introduce data on the emerging science of inflammation-driven posttranslational modifications on proteins responsible for driving growth, angiogenesis, immunosuppression, and inhibition of apoptosis. Examples include data from human melanoma, breast, head and neck, lung, and colon cancers. Fortunately, numerous antioxidant agents are clinically available, and we further propose that the pharmacologic attenuation of these inflammatory processes, particularly the reactive nitrogen species, will restore the cancer cells to an apoptosis-permissive and growth-inhibitory state. Our mouse model data using an arginine antagonist that prevents enzymatic production of nitric oxide directly supports this view. We contend that selected antioxidants be considered as part of the cancer treatment approach, as they are likely to provide a novel and mechanistically justified addition for therapeutic benefit.

Indexed as

Signal TransductionAnimalsAntineoplastic AgentsApoptosisHumansInflammationMelanomaNeoplasmsNitric OxideOxidation-ReductionTranslational Research, BiomedicalTumor MicroenvironmentAntineoplastic AgentsNitric Oxide

Identifiers

PMID23868870
PMCPMC3873873

What OpenQuestion holds

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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.