Evidence map›Paper›PMID 30694461›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2019

Distinct prognostic values of Annexin family members expression in acute myeloid leukemia.

Y Niu, X Yang, Y Chen, X Jin, Y Xie, Y Tang, L Li, S Liu, Y Guo, X Li and 2 more

Abstract read
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Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Annexin A13 Protects Against Acute Kidney Injury by Inactivating TGF-β/Smad3 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

12 authors at 2 institutions in 1 country.

Y NiuHenan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, People's Republic of China.
X YangHenan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, People's Republic of China.
Y ChenHenan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, People's Republic of China.
X JinHenan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, People's Republic of China.
Y XieHenan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, People's Republic of China.
Y TangLaboratory of Hematology, The First Affiliated Hospital of Xinxiang Medical University, Weihui, 453003, Henan, People's Republic of China.
L LiHenan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, People's Republic of China.
S LiuHenan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, People's Republic of China.
Y GuoHenan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, People's Republic of China.
X LiHenan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, People's Republic of China.
L DuanHenan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, People's Republic of China.
H WangHenan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, People's Republic of China. wanghui@xxmu.edu.cn.ORCID http://orcid.org/0000-0002-2454-3814
Xinxiang Medical University · CNFirst Affiliated Hospital of Xinxiang Medical University · CN

Funding

National Natural Science Foundation of China 81701554National Natural Science Foundation of China 81702099Natural Science Foundation of Henan Province 162300410213
6 · The paper itself

Abstract

backgroundAnnexin family consist of 12 members, many of them are frequently dysregulated in human cancers. However, the diagnosis and prognosis of Annexin family expression in acute myeloid leukemia (AML) remain elusive. The aim of the present study was to assess the prognostic value of Annexin expressions in adult and pediatric AML.

methodsGenomicScape tool was used to assess the prognostic value of the expressions of Annexin family members in a cohort of 162 adult AML patients. Quantitative reverse transcript real-time PCR (QRT-PCR) was performed to detect the ANXA2 expression level in the bone marrow-derived mononuclear cells (BMMCs) obtained from 101 pediatric AML patients and 30 controls.

resultsThe results demonstrated that high mRNA expressions of ANXA2, ANXA6, and ANXA7 were significantly associated with worse prognosis, while ANXA5 was correlated with better prognosis in adult AML. QRT-PCR analysis showed that ANXA2 expression was dramatically downregulated in BMMCs of pediatric AML patients compared to controls (p < 0.0001). ROC analysis demonstrated that ANXA2 could efficiently differentiate pediatric AML patients from controls (AUC 0.872, p < 0.0001). Likewise, ANXA2 was significantly lower in AML patients with poor-risk karyotype (p = 0.048). Also, the level of ANXA2 trended to decrease in AML patients who had not achieving complete remission. Moreover, patients with lower expression of ANXA2 had higher death rate (p = 0.042) and shorter overall survival (HR 0.55, p = 0.042). Thus, these findings suggest that ANXA2 exerts poor prognostic effect on adult AML but favorable prognostic effect on pediatric AML.

conclusionsCollectively, Annexin family members exert distinct prognostic roles in AML, and ANXA2 can be used as a biological marker for diagnosis and prognosis of pediatric AML.

Indexed as

AdolescentAnnexinsBiomarkers, TumorChildChild, PreschoolComputational BiologyDatabases, FactualFemaleGene Expression ProfilingHumansInfantLeukemia, Myeloid, AcuteMaleNeoplasm Recurrence, LocalPrognosisSurvival RateAnnexinsBiomarkers, TumorAcute myeloid leukemiaAnnexin familyANXA2Prognostic biomarker

Identifiers

PMID30694461
OpenAlexW2913292440

What OpenQuestion holds

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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.