Evidence map›Paper›PMID 38890503›Full record

ArticleCommunications biology2024

Androgen-responsive FOXP4 is a target for endometrial carcinoma.

Kayo Kayahashi, Mahadi Hasan, Anowara Khatun, Susumu Kohno, Jumpei Terakawa, Shin-Ichi Horike, Natsumi Toyoda, Ayumi Matsuoka, Takashi Iizuka, Takeshi Obata and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2024. 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
–field-weighted citation impact
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. 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

15 authors.

Kayo KayahashiDepartment of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Mahadi HasanDivision of Animal Disease Model, Research Center for Experimental Modeling of Human Disease, Kanazawa University, Kanazawa, Japan.
Anowara KhatunDivision of Animal Disease Model, Research Center for Experimental Modeling of Human Disease, Kanazawa University, Kanazawa, Japan.
Susumu KohnoCancer Research Institute, Kanazawa University, Kanazawa, Japan.
Jumpei TerakawaGraduate School of Veterinary Science, Azabu University, Sagamihara, Japan.
Shin-Ichi HorikeDivision of Integrated Omics Research, Research Center for Experimental Modeling of Human Disease, Kanazawa University, Kanazawa, Japan.
Natsumi ToyodaDivision of Animal Disease Model, Research Center for Experimental Modeling of Human Disease, Kanazawa University, Kanazawa, Japan.
Ayumi MatsuokaDepartment of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Takashi IizukaDepartment of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.ORCID 0000-0003-1885-6272
Takeshi ObataDepartment of Obstetrics and Gynecology, Toyama Prefectural Central Hospital, Toyama, Japan.
Masanori OnoDepartment of Obstetrics and Gynecology, Tokyo Medical University, Nishi-Shinjuku, Japan.ORCID 0000-0001-9249-6813
Yasunari MizumotoDepartment of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Chiaki TakahashiCancer Research Institute, Kanazawa University, Kanazawa, Japan.ORCID 0000-0003-3390-9563
Hiroshi FujiwaraDepartment of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan. fuji@med.kanazawa-u.ac.jp.ORCID 0000-0003-3098-9406
Takiko DaikokuDivision of Animal Disease Model, Research Center for Experimental Modeling of Human Disease, Kanazawa University, Kanazawa, Japan. tdaikoku@kiea.m.kanazawa-u.ac.jp.ORCID 0000-0002-6280-8502

Funding

Japan Agency for Medical Research and Development (AMED) 22ck0106549h0001
6 · The paper itself

Abstract

Although low estrogen is considered to suppress uterine endometrial carcinoma, the most cases occur in the postmenopausal stage. After menopause, the production of androgen level also declines. Therefore, to resolve the above enigma, we hypothesize that the postmenopausal decline of androgen is a trigger of its progression. In the present study, to validate this hypothesis, we examine the pathological roles of androgen/AR by analyzing clinical data, culturing endometrioid cancer cell lines, and using murine models. Clinical data show that androgen receptor (AR) expression and serum dihydrotestosterone (DHT) are associated with lower disease-free survival (DFS). DHT suppresses malignant behaviors in AR-transfected human endometrial cancer cells (ECC). In ovariectomized Pten

Indexed as

AndrogensEndometrial NeoplasmsForkhead Transcription FactorsReceptors, AndrogenAnimalsCell Line, TumorCell ProliferationDihydrotestosteroneFemaleGene Expression Regulation, NeoplasticHumansMiceMiddle AgedAndrogensDihydrotestosteroneForkhead Transcription FactorsReceptors, Androgen

Identifiers

PMID38890503
PMCPMC11189448

What OpenQuestion holds

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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.