Evidence map›Paper›PMID 23715741›Full record

ReviewJournal of leukocyte biology2013

Novel roles of reactive oxygen species in the pathogenesis of acute myeloid leukemia.

Fuling Zhou, Qiang Shen, François X Claret

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
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  7. Role of reactive oxygen species in myelodysplastic syndromes.Cellular & molecular biology letters · 2024
    Review
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  19. A novel immune prognostic model of non-M3 acute myeloid leukemia.American journal of translational research · 2022
    Article
  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 at 2 institutions in 2 countries.

Fuling ZhouDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Qiang Shen
François X Claret
Second Affiliated Hospital of Xi'an Jiaotong University · CNThe University of Texas MD Anderson Cancer Center · US

Funding

Targeting JAB1 Oncogenic Function in Breast CancerR01CA090853 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI CLARET, FRANCOIS X · 2002 to 2011
$2.5M
NCI NIH HHS R01 CA090853NCI NIH HHS R01-CA90853
6 · The paper itself

Abstract

It has become apparent that regulation of ROS is important in cell signaling and homeostasis. Accumulation of ROS triggers oxidative stress in various cell types and contributes to the development, progression, and persistence of cancer. Recent research has demonstrated that redox dysregulation caused by ROS promotes proliferation, differentiation, genomic, and epigenetic alterations; immune evasion; and survival in leukemic cells. ROS act as signaling molecules to regulate redox-sensitive transcriptional factors, enzymes, oncogenes, and other downstream effectors. Thus, a thorough understanding the role of ROS as key mediators in leukemogenesis is likely to provide opportunities for improved pharmacological intervention. In this review, we summarize the recent findings that support a role for ROS in the pathogenesis of AML and outline innovative approaches in the implementation of redox therapies for myeloid malignancies.

Indexed as

CytokinesDNA DamageGene Expression Regulation, LeukemicHematopoietic Stem CellsHumansLeukemia, Myeloid, AcuteMitochondriaReactive Oxygen SpeciesTumor EscapeCytokinesReactive Oxygen Speciescell signalingleukemogenesisROS

Identifiers

PMID23715741
PMCPMC4051257
OpenAlexW2147749058

What OpenQuestion holds

Textmetadata
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.