Evidence map›Paper›PMID 36273006›Full record

ArticleNature communications2022

Single-cell transcriptomic analysis highlights origin and pathological process of human endometrioid endometrial carcinoma.

Xiaojun Ren, Jianqing Liang, Yiming Zhang, Ning Jiang, Yuhui Xu, Mengdi Qiu, Yiqin Wang, Bing Zhao, Xiaojun Chen

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 2 pooled it
9.1field-weighted citation impact, top 1% 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

70 citing papers in PubMed, 2 syntheses or guidelines pooled it, 109 citations in OpenAlex.

  1. Pooled it
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  10. Multi-Omics Data Reveal Estrogen-Driven Dysregulation and Stromal-Epithelial Signaling Alterations in Endometrial Polyps.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  12. Involvement of increased arginase-1The Journal of international medical research · 2026
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10 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

Xiaojun Ren *Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China.
Jianqing Liang *State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Yiming Zhang *State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Ning Jiang *State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Yuhui XuObstetrics and Gynecology Hospital of Fudan University, Shanghai, China.
Mengdi QiuState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Yiqin WangObstetrics and Gynecology Hospital of Fudan University, Shanghai, China.
Bing ZhaoState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China. bingzhao@fudan.edu.cn.ORCID 0000-0001-9891-3569
Xiaojun ChenObstetrics and Gynecology Hospital of Fudan University, Shanghai, China. chenxiaojun1366@fckyy.org.cn.ORCID 0000-0002-5493-1500
Obstetrics and Gynecology Hospital of Fudan University · CNSun Yat-sen University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometrial cancers are complex ecosystems composed of cells with distinct phenotypes, genotypes, and epigenetic states. Current models do not adequately reflect oncogenic origin and pathological progression in patients. Here we use single-cell RNA sequencing to profile cells from normal endometrium, atypical endometrial hyperplasia, and endometrioid endometrial cancer (EEC), which altogether represent the step-by-step development of endometrial cancer. We find that EEC originates from endometrial epithelial cells but not stromal cells, and unciliated glandular epithelium is the source of EEC. We also identify LCN2 + /SAA1/2 + cells as a featured subpopulation of endometrial tumorigenesis. Finally, the stromal niche and immune environment changes during EEC progression are described. This study elucidates the evolution of cell populations in EEC development at single-cell resolution, which would provide a direction to facilitate EEC research and diagnosis.

Indexed as

Carcinoma, EndometrioidEndometrial HyperplasiaEndometrial NeoplasmsEcosystemFemaleHumansTranscriptome

Identifiers

PMID36273006
PMCPMC9588071
OpenAlexW4307139533

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.