Evidence map›Paper›PMID 32617298›Full record

ArticleAnnals of translational medicine2020

Identification the prognostic value of glutathione peroxidases expression levels in acute myeloid leukemia.

Jie Wei, Qiongni Xie, Xinran Liu, Chengyao Wan, Wenqi Wu, Kuiyan Fang, Yibin Yao, Peng Cheng, Donghong Deng, Zhenfang Liu

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.1field-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

60 citing papers in PubMed, 95 citations in OpenAlex.

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  3. Macrophage ferroptosis in hematologic malignancies: emerging mechanisms and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026
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  11. Ferroptosis: a novel therapeutic warrior in the battle against leukemia.Apoptosis : an international journal on programmed cell death · 2025
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Glutathione-Dependent Pathways in Cancer Cells.International journal of molecular sciences · 2024
    Review
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  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

10 authors at 2 institutions in 1 country.

Jie WeiDepartment of Hematology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Qiongni XieDepartment of Hematology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Xinran LiuDepartment of Hematology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Chengyao WanDepartment of Hematology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Wenqi WuDepartment of Hematology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Kuiyan FangDepartment of Hematology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Yibin YaoDepartment of Hematology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Peng ChengDepartment of Hematology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Donghong DengDepartment of Hematology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Zhenfang LiuDepartment of Hematology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
First Affiliated Hospital of GuangXi Medical University · CNGuangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlutathione peroxidases (GPXs) are an enzyme family with peroxidase activity. Abnormal GPX expression is associated with carcinogenesis. However, the potential role of the GPX gene family in acute myeloid leukemia (AML) remains to be comprehensively examined.

methodsWe analyzed GPX mRNA expression levels and determined the correlation between gene expression and the prognostic value via multiple universally acknowledged databases including the Oncomine, Gene Expression Profiling Interactive Analysis (GEPIA), PROGgeneV2, UALCAN, Cancer Cell Line Encyclopedia (CCLE), and The European Bioinformatics Institute (EMBL-EBI) databases. The functional network of differentially expressed GPXs was investigated via the NetworkAnalyst platform. Correlated genes as well as kinase, microRNA (miRNA), and transcription factor (TF) targets were identified using LinkedOmics.

resultsWe observed that the transcriptional expression levels of GPX-1, -2, -4, -7, and -8 had significant difference between AML patients samples and normal samples, and that AML patients with high expression of GPX-1, -3, -4, and -7 were associated with poorer prognosis of overall survival (OS). Functional enrichment analysis showed that the differentially expressed GPXs were mainly enriched in response to oxidative stress, regulation of immune response, and inflammatory response, along with glutathione metabolism and ferroptosis. Overexpression of correlated genes, PSMB10, VPS13D, NDUFS8, ATP5D, POLR2E, and HADH were linked to adverse OS in AML. Regulatory network analysis indicated that differentially expressed GPXs regulated cell proliferation, cancer progression, apoptosis, and cell cycle signaling via pathways involving cancer-related kinases (such as DAPK1 and SRC), miRNAs (such as miR-202 and miR-181), and TFs (such as SRF and E2F1).

conclusionsOur findings offer novel insights into the differential expression and prognostic potential of the GPX family in AML, and lay a foundation for subsequent research of GPX's role in the carcinogenesis and regulatory network of AML.

Indexed as

Acute myeloid leukemia (AML)bioinformatics analysisfunctional networkglutathione peroxidases (GPXs)prognosis

Identifiers

PMID32617298
PMCPMC7327321
OpenAlexW3029628311

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.