Evidence map›Paper›PMID 35172562›Full record

ArticleHaematologica2022

The NADPH oxidase NOX2 is a marker of adverse prognosis involved in chemoresistance of acute myeloid leukemias.

Rosa Paolillo, Mathias Boulanger, Pierre Gâtel, Ludovic Gabellier, Marion De Toledo, Denis Tempé, Rawan Hallal, Dana Akl, Jérôme Moreaux, Hayeon Baik and 6 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

30 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  6. A multi-omics integrative analyses revealsFrontiers in pharmacology · 2026
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  8. Identification of Differentially Expressed Genes and SNPs Linked toInternational journal of molecular sciences · 2025
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  10. Review
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  12. NOX Family: Regulators of Reactive Oxygen Species Balance in Tumor Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 5 institutions in 1 country.

Rosa PaolilloIGMM, Univ Montpellier, CNRS, Montpellier, France; Equipe labellisée Ligue Contre le Cancer, Paris.
Mathias BoulangerIGMM, Univ Montpellier, CNRS, Montpellier, France; Equipe labellisée Ligue Contre le Cancer, Paris.
Pierre GâtelIGMM, Univ Montpellier, CNRS, Montpellier, France; Equipe labellisée Ligue Contre le Cancer, Paris.
Ludovic GabellierIGMM, Univ Montpellier, CNRS, Montpellier, France; Equipe labellisée Ligue Contre le Cancer, Paris, France; Département d'Hématologie Clinique, CHU de Montpellier, Montpellier.
Marion De ToledoIGMM, Univ Montpellier, CNRS, Montpellier, France; Equipe labellisée Ligue Contre le Cancer, Paris.
Denis TempéIGMM, Univ Montpellier, CNRS, Montpellier, France; Equipe labellisée Ligue Contre le Cancer, Paris.
Rawan HallalIGMM, Univ Montpellier, CNRS, Montpellier, France; Equipe labellisée Ligue Contre le Cancer, Paris.
Dana AklIGMM, Univ Montpellier, CNRS, Montpellier, France; Equipe labellisée Ligue Contre le Cancer, Paris.
Jérôme MoreauxIGH, Univ Montpellier, CNRS, Montpellier.
Hayeon BaikIGMM, Univ Montpellier, CNRS, Montpellier, France; Equipe labellisée Ligue Contre le Cancer, Paris.
Elise GueretMGX, Univ Montpellier, CNRS, INSERM, Montpellier.
Christian RecherService d'Hématologie, CHU de Toulouse, Toulouse, France; CRCT, University of Toulouse, INSERM, CNRS, Toulouse.
Jean-Emmanuel SarryCRCT, University of Toulouse, INSERM, CNRS, Toulouse.
Guillaume CartronDépartement d'Hématologie Clinique, CHU de Montpellier, Montpellier.
Marc PiechaczykIGMM, Univ Montpellier, CNRS, Montpellier, France; Equipe labellisée Ligue Contre le Cancer, Paris.
Guillaume BossisIGMM, Univ Montpellier, CNRS, Montpellier, France; Equipe labellisée Ligue Contre le Cancer, Paris. guillaume.bossis@igmm.cnrs.fr.
Centre National de la Recherche Scientifique · FRLa Ligue Contre le Cancer · FRUniversité de Montpellier · FRCentre Hospitalier Universitaire de Montpellier · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resistance to chemotherapeutic drugs is a major cause of treatment failure in acute myeloid leukemias (AML). To better characterize the mechanisms of chemoresistance, we first identified genes whose expression is dysregulated in AML cells resistant to daunorubicin or cytarabine, the main drugs used for induction therapy. The genes found to be activated are mostly linked to immune signaling and inflammation. Among them, we identified a strong upregulation of the NOX2 NAPDH oxidase subunit genes (CYBB, CYBA, NCF1, NCF2, NCF4 and RAC2). The ensuing increase in NADPH oxidase expression and production of reactive oxygen species, which is particularly strong in daunorubicin-resistant cells, participates in the acquisition and/or maintenance of resistance to daunorubicin. Gp91phox (CYBB-encoded Nox2 catalytic subunit), was found to be more expressed and active in leukemic cells from patients with the French-American-British (FAB) M4/M5 subtypes of AML than in those from patients with the FAB M0-M2 ones. Moreover, its expression was increased at the surface of patients' chemotherapy-resistant AML cells. Finally, using a gene expression based score we demonstrated that high expression of NOX2 subunit genes is a marker of adverse prognosis in AML patients. The prognostic NOX score we defined is independent of the cytogenetic-based risk classification, FAB subtype, FLT3/NPM1 mutational status and age.

Indexed as

Leukemia, Myeloid, AcuteNADPH Oxidase 2DaunorubicinDrug Resistance, NeoplasmHumansPrognosisCYBB protein, humanDaunorubicinNADPH Oxidase 2

Identifiers

PMID35172562
PMCPMC9614539
OpenAlexW4225365552

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.