Evidence map›Paper›PMID 38103082›Full record

ArticleCellular and molecular life sciences : CMLS2023

miR-181a plays the tumor-suppressor role in chronic myeloid leukemia CD34

Xiuyan Zhang, Wenjuan Ma, Wen Xue, Yu Wang, Pan Chen, Quanxue Li, Yuan-Yuan Li, Xiaohui Hu, Yun Zhao, Haixia Zhou

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. MircoRNAs predict and modulate responses to chemotherapy in leukemic patients.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  5. Article
  6. Review
  7. 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 1 institution in 1 country.

Xiuyan Zhang *Cyrus Tang Medical Institute, Collaborative Innovation Center of Hematology, Soochow University, Suzhou, 215123, China. zhangxiuyan@suda.edu.cn.
Wenjuan MaCyrus Tang Medical Institute, Collaborative Innovation Center of Hematology, Soochow University, Suzhou, 215123, China.
Wen XueCyrus Tang Medical Institute, Collaborative Innovation Center of Hematology, Soochow University, Suzhou, 215123, China.
Yu WangCyrus Tang Medical Institute, Collaborative Innovation Center of Hematology, Soochow University, Suzhou, 215123, China.
Pan ChenCyrus Tang Medical Institute, Collaborative Innovation Center of Hematology, Soochow University, Suzhou, 215123, China.
Quanxue LiShanghai-MOST Key Laboratory of Health and Disease Genomics, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai, 200237, China.
Yuan-Yuan LiShanghai-MOST Key Laboratory of Health and Disease Genomics, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai, 200237, China.
Xiaohui Hu *The First Affiliated Hospital of Soochow University, Key Laboratory of Thrombosis and Hemostasis, Ministry of Health, Suzhou, 215006, China. hxh27@163.com.
Yun Zhao *Cyrus Tang Medical Institute, Collaborative Innovation Center of Hematology, Soochow University, Suzhou, 215123, China. zhaoy@suda.edu.cn.
Haixia Zhou *The First Affiliated Hospital of Soochow University, Key Laboratory of Thrombosis and Hemostasis, Ministry of Health, Suzhou, 215006, China. zhouhaixia@suda.edu.cn.ORCID http://orcid.org/0009-0001-5309-5715
Soochow University · CN

Funding

National Natural Science Foundation of China 32070793National Natural Science Foundation of China 81800151National Natural Science Foundation of China 82270191
6 · The paper itself

Abstract

The formation of the BCR-ABL fusion gene drives human chronic myeloid leukemia (CML). The last 2 decades have witnessed that specific tyrosine kinase inhibitors (TKIs, e.g., imatinib mesylate, IM) against ABL1 improve disease treatment, although some patients still suffer from relapse and TKI resistance. Therefore, a better understanding of the molecular pathology of CML is still urgently needed. miR-181a-5p (miR-181a) acts as a tumor suppressor in CML; however, the molecular mechanism of miR-181a in CML stem/progenitor cells remains elusive. Herein, we showed that miR-181a inhibited the growth of CML CD34

Indexed as

Leukemia, Myelogenous, Chronic, BCR-ABL PositiveMicroRNAsPlasminogen Activator Inhibitor 1ApoptosisDrug Resistance, NeoplasmFusion Proteins, bcr-ablHumansImatinib MesylateProtein Kinase InhibitorsFusion Proteins, bcr-ablImatinib MesylateMicroRNAsMIrn181 microRNA, humanPlasminogen Activator Inhibitor 1Protein Kinase InhibitorsSERPINE1 protein, humanCD34+ cellsChronic myeloid leukemiaImatinib mesylatemiR-181aSERPINE1

Identifiers

PMID38103082
PMCPMC10725356
OpenAlexW4389832030

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.