Evidence map›Paper›PMID 19380816›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Mechanism regulating reactive oxygen species in tumor-induced myeloid-derived suppressor cells.

Cesar A Corzo, Matthew J Cotter, Pingyan Cheng, Fendong Cheng, Sergei Kusmartsev, Eduardo Sotomayor, Tapan Padhya, Thomas V McCaffrey, Judith C McCaffrey, Dmitry I Gabrilovich

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04150900 (1922GCCC), which is not on this map. Cited by 470 papers.

0numbers the graph read from it
0cells of the map it votes in
470citing papers in PubMed
12.6field-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.

NCT04150900 phase2active not recruitingnot on this mapstarted 2020, after this paper: background citation

1922gccc: phase 2 study of pembrolizumab and bavituximab for progressive recurrent/metastatic squamous cell carcinoma of the head and neck

TypeinterventionalSponsorUniversity of Maryland, BaltimoreRan2020 to 2027Enrolled7ConditionsSquamous Cell CarcinomaArmsBavituximab, Pembrolizumab
3 · Its place in the literature

Who cites it

470 citing papers in PubMed, 744 citations in OpenAlex.

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  12. Redox processes in the treatment of advanced skin cancers.Clinical & experimental metastasis · 2026
    Review
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  14. Review
  15. Review
  16. Targeting innate immunity to overcome immune evasion in HPV-associated cancers.Frontiers in cellular and infection microbiology · 2026
    Review
  17. Review
  18. Metabolic Checkpoints in CD8International journal of biological sciences · 2026
    Review
  19. Article
  20. Review

410 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

10 authors at 2 institutions in 1 country.

Cesar A CorzoH. Lee Moffitt Cancer Center and Research Institute, University of South Florida, Tampa, FL, 33612, USA.
Matthew J Cotter
Pingyan Cheng
Fendong Cheng
Sergei Kusmartsev
Eduardo Sotomayor
Tapan Padhya
Thomas V McCaffrey
Judith C McCaffrey
Dmitry I Gabrilovich
Moffitt Cancer Center · USUniversity of South Florida · US

Funding

Correction of myeloid cell defects in cancerR01CA084488 · NCI · WISTAR INSTITUTE · PI GABRILOVICH, DMITRY I · 1999 to 2017
$5.4M
Mechanisms of Immune Suppression in CancerF31CA123708 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI CORZO, CESAR ALEXANDER · 2007 to 2009
$90k
NCI NIH HHS 1R01 CA 84488NCI NIH HHS F31 CA123708NCI NIH HHS F31 CA 123708-02NCI NIH HHS R01 CA084488
6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSC) are a major component of the immune suppressive network described in cancer and many other pathological conditions. Recent studies have demonstrated that one of the major mechanisms of MDSC-induced immune suppression is mediated by reactive oxygen species (ROS). However, the mechanism of this phenomenon remained unknown. In this study, we observed a substantial up-regulation of ROS by MDSC in all of seven different tumor models and in patients with head and neck cancer. The increased ROS production by MDSC is mediated by up-regulated activity of NADPH oxidase (NOX2). MDSC from tumor-bearing mice had significantly higher expression of NOX2 subunits, primarily p47(phox) and gp91(phox), compared with immature myeloid cells from tumor-free mice. Expression of NOX2 subunits in MDSC was controlled by the STAT3 transcription factor. In the absence of NOX2 activity, MDSC lost the ability to suppress T cell responses and quickly differentiated into mature macrophages and dendritic cells. These findings expand our fundamental understanding of the biology of MDSC and may also open new opportunities for therapeutic regulation of these cells in cancer.

Indexed as

AgedAnimalsCarcinoma, Lewis LungCell LineCell Line, TumorHumansMembrane GlycoproteinsMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicMiddle AgedMyeloid CellsNADPH Oxidase 2NADPH OxidasesCybb protein, mouseMembrane GlycoproteinsNADPH Oxidase 2NADPH OxidasesReactive Oxygen SpeciesStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID19380816
PMCPMC2833019
OpenAlexW2128957395

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.