Evidence map›Paper›PMID 32868822›Full record

ArticleScientific reports2020

ARID1A protein expression is retained in ovarian endometriosis with ARID1A loss-of-function mutations: implication for the two-hit hypothesis.

Nozomi Yachida, Kosuke Yoshihara, Kazuaki Suda, Hirofumi Nakaoka, Haruka Ueda, Kentaro Sugino, Manako Yamaguchi, Yutaro Mori, Kaoru Yamawaki, Ryo Tamura and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  7. Pathogenesis of Endometriosis and Endometriosis-Associated Cancers.International journal of molecular sciences · 2024
    Review
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  12. Article
  13. The Emerging Role of Chromatin Remodeling Complexes in Ovarian Cancer.International journal of molecular sciences · 2022
    Review
  14. Article
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  16. Article
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  18. Article
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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

15 authors at 3 institutions in 1 country.

Nozomi YachidaDepartment of Obstetrics and Gynecology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ward, Niigata, 951-8510, Japan.
Kosuke YoshiharaDepartment of Obstetrics and Gynecology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ward, Niigata, 951-8510, Japan. yoshikou@med.niigata-u.ac.jp.
Kazuaki SudaDepartment of Obstetrics and Gynecology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ward, Niigata, 951-8510, Japan.
Hirofumi NakaokaHuman Genetics Laboratory, National Institute of Genetics, Mishima, 411-8540, Japan.
Haruka UedaDepartment of Obstetrics and Gynecology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ward, Niigata, 951-8510, Japan.
Kentaro SuginoDepartment of Obstetrics and Gynecology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ward, Niigata, 951-8510, Japan.
Manako YamaguchiDepartment of Obstetrics and Gynecology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ward, Niigata, 951-8510, Japan.
Yutaro MoriDepartment of Obstetrics and Gynecology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ward, Niigata, 951-8510, Japan.
Kaoru YamawakiDepartment of Obstetrics and Gynecology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ward, Niigata, 951-8510, Japan.
Ryo TamuraDepartment of Obstetrics and Gynecology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ward, Niigata, 951-8510, Japan.
Tatsuya IshiguroDepartment of Obstetrics and Gynecology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ward, Niigata, 951-8510, Japan.
Masanori IsobeDepartment of Obstetrics and Gynecology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ward, Niigata, 951-8510, Japan.
Teiichi MotoyamaDepartment of Molecular and Diagnostic Pathology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, 951-8510, Japan.
Ituro InoueHuman Genetics Laboratory, National Institute of Genetics, Mishima, 411-8540, Japan.
Takayuki EnomotoDepartment of Obstetrics and Gynecology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ward, Niigata, 951-8510, Japan.
Niigata University Medical and Dental Hospital · JPNational Institute of Genetics · JPNiigata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ARID1A loss-of-function mutation accompanied by a loss of ARID1A protein expression is considered one of the most important driver events in endometriosis-associated ovarian cancer. Although our recent genomic study clarified that ARID1A loss-of-function mutations were detected in 13% of ovarian endometriosis, an association between the ARID1A mutation status and ARID1A protein expression in ovarian endometriosis remains unclear. We performed immunohistochemical staining for ARID1A in 78 ovarian endometriosis samples and 99 clear cell carcinoma samples. We revealed that not only 70 endometriosis samples without ARID1A mutations but also eight endometriosis samples with ARID1A loss-of-function mutations retained ARID1A protein expression. On the other hand, most of clear cell carcinomas with ARID1A loss-of-function mutations showed a loss of ARID1A protein expression. In particular, clear cell carcinoma samples which harbor multiple ARID1A loss-of-function mutations or both a single ARID1A loss-of-function mutation and ARID1A allelic imbalance lost ARID1A protein expression. However, ARID1A protein expression was retained in seven clear cell carcinomas with ARID1A loss-of-function mutations. These results suggest that a single ARID1A loss-of-function mutation is insufficient for ARID1A loss in ovarian endometriosis and some clear cell carcinoma. Further driver events may be needed for the malignant transformation of ovarian endometriosis with ARID1A loss-of-function mutations.

Indexed as

Adenocarcinoma, Clear CellDNA-Binding ProteinsEndometriosisFemaleGene ExpressionGenetic Predisposition to DiseaseHumansLoss of Function MutationOvarian DiseasesOvarian NeoplasmsTranscription FactorsARID1A protein, humanDNA-Binding ProteinsTranscription Factors

Identifiers

PMID32868822
PMCPMC7459315
OpenAlexW3081868588

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LicenceCC BY
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Registered trials

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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.