Evidence map›Paper›PMID 35842445›Full record

ArticleCell death discovery2022

Estrogens revert neutrophil hyperplasia by inhibiting Hif1α-cMyb pathway in zebrafish myelodysplastic syndromes models.

Xuexiao Li, Luping Wang, Xun Qin, Xiaohui Chen, Li Li, Zhibin Huang, Wenqing Zhang, Wei Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
  2. 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

8 authors at 3 institutions in 1 country.

Xuexiao Li *Key Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases of Guangdong Higher Education Institutes, Department of Developmental Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510006, People's Republic of China.
Luping Wang *Division of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou, 510006, People's Republic of China.
Xun QinKey Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases of Guangdong Higher Education Institutes, Department of Developmental Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510006, People's Republic of China.
Xiaohui ChenDivision of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou, 510006, People's Republic of China.
Li LiDivision of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou, 510006, People's Republic of China.
Zhibin HuangDivision of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou, 510006, People's Republic of China.
Wenqing ZhangKey Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases of Guangdong Higher Education Institutes, Department of Developmental Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510006, People's Republic of China. mczhangwq@scut.edu.cn.ORCID http://orcid.org/0000-0002-3636-7133
Wei LiuDivision of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou, 510006, People's Republic of China. liuwei7@scut.edu.cn.ORCID http://orcid.org/0000-0003-3660-5514
South China University of Technology · CNSouthern Medical University · CNZhujiang Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81770167
6 · The paper itself

Abstract

Myelodysplastic syndromes (MDS) are characterized by daunting genetic heterogeneity and a high risk of leukemic transformation, which presents great challenges for clinical treatment. To identify new chemicals for MDS, we screened a panel of FDA-approved drugs and verified the neutrophil hyperplasia inhibiting role of 17β-estradiol (E2, a natural estrogen) in several zebrafish MDS models (pu.1

Identifiers

PMID35842445
PMCPMC9288432
OpenAlexW4285588601

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.