Evidence map›Paper›PMID 38572589›Full record

ArticleClinical and translational medicine2024

m

Yanchun Zhao, Yutong Zhou, Yu Qian, Wenwen Wei, Xiangjie Lin, Shihui Mao, Jie Sun, Jie Jin

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
4.4field-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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
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  3. Ubiquitination and NOncology letters · 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

8 authors at 1 institution in 1 country.

Yanchun ZhaoDepartment of Hematology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Yutong ZhouDepartment of Hematology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Yu QianDepartment of Hematology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Wenwen WeiDepartment of Hematology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Xiangjie LinDepartment of Hematology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Shihui MaoDepartment of Hematology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Jie SunDepartment of Hematology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Jie JinDepartment of Hematology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.ORCID 0000-0002-8166-9915
Zhejiang Cancer Hospital · CN

Funding

Key Research and Development Program of Zhejiang 2021C03123National Natural Science Foundation of China 81820108004National Natural Science Foundation of China 82170144Research Project of Jinan Microecological Biomedicine Shandong Laboratory JNL-2022034C
6 · The paper itself

Abstract

backgroundAcute myeloid leukaemia (AML) is a haematological malignancy with unfavourable prognosis. Despite the effectiveness of chemotherapy and targeted therapy, relapse or drug resistance remains a major threat to AML patients. N6-methyladenosine (m

methodsChromatin immunoprecipitation (ChIP) sequencing data from Gene Expression Omnibus (GEO) cohort were analysed to search SE-related genes. The mechanisms of m

resultsWe identified two SE-associated transcripts IGF2BP2 and IGF2BP3 in AML. High enrichment of H3K27ac, H3K4me1 and BRD4 was observed in IGF2BP2 and IGF2BP3, whose expression were driven by SE machinery. Then IGF2BP2 and IGF2BP3 enhanced the stability of DDX21 mRNA in an m

conclusionsDysregulation of SE-IGF2BP2/IGF2BP3-DDX21 axis facilitated the progression of AML. Our findings provide new insights into the link between SEs and m

Indexed as

Leukemia, Myeloid, AcuteNuclear ProteinsBromodomain Containing ProteinsCell Cycle ProteinsDEAD-box RNA HelicasesHumansNeoplasm Recurrence, LocalRNARNA-Binding ProteinsTranscription FactorsUp-RegulationBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsDDX21 protein, humanDEAD-box RNA HelicasesIGF2BP2 protein, humanIGF2BP3 protein, humanNuclear ProteinsRNARNA-Binding ProteinsTranscription Factorsacute myeloid leukaemia (AML)DDX21N6‐methyladenosine (m6A)super‐enhancers (SEs)

Identifiers

PMID38572589
PMCPMC10993053
OpenAlexW4393948258

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.