Evidence map›Paper›PMID 27499903›Full record

ArticleThe journal of pathology. Clinical research2015

Increased proliferation in atypical hyperplasia/endometrioid intraepithelial neoplasia of the endometrium with concurrent inactivation of ARID1A and PTEN tumour suppressors.

Ayse Ayhan, Tsui-Lien Mao, Yohan Suryo Rahmanto, Felix Zeppernick, Hiroshi Ogawa, Ren-Chin Wu, Tian-Li Wang, Ie-Ming Shih

Open access · goldAbstract read
In one paragraph

Article in The journal of pathology. Clinical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

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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

8 authors at 4 institutions in 4 countries.

Ayse AyhanDepartment of PathologyJohns Hopkins Medical InstitutionsBaltimoreMaryland; Department of PathologyHamamatsu University School of Medicine and Seirei Mikatahara HospitalHamamatsuJapan.
Tsui-Lien MaoDepartment of Pathology National Taiwan University College of Medicine Taipei Taiwan.
Yohan Suryo RahmantoDepartment of Pathology Johns Hopkins Medical Institutions Baltimore Maryland.
Felix ZeppernickDepartment of PathologyJohns Hopkins Medical InstitutionsBaltimoreMaryland; Department of Gynecology and ObstetricsUniversity Hospital AachenGermany.
Hiroshi OgawaDepartment of Pathology Hamamatsu University School of Medicine and Seirei Mikatahara Hospital Hamamatsu Japan.
Ren-Chin WuDepartment of PathologyJohns Hopkins Medical InstitutionsBaltimoreMaryland; Department of PathologyChang Gung Memorial Hospital and Chang Gung University College of MedicineTaoyuanTaiwan.
Tian-Li WangDepartment of Pathology Johns Hopkins Medical Institutions Baltimore Maryland.
Ie-Ming ShihDepartment of PathologyJohns Hopkins Medical InstitutionsBaltimoreMaryland; Department of Gynecology and ObstetricsJohns Hopkins Medical InstitutionsBaltimoreMaryland.
Johns Hopkins University · USNational Taiwan University · TWSeirei Hamamatsu General Hospital · JPSeirei Mikatabara General Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uterine endometrioid carcinoma is the most common neoplastic disease in the female genital tract and develops from a common precursor lesion, atypical hyperplasia/endometrioid intraepithelial neoplasia (AH/EIN). Although the genomic landscape of endometrioid carcinoma has been recently revealed, the molecular alterations that contribute to tumour progression from AH/EIN to carcinoma remain to be elucidated. In this study, we used immunohistochemistry to determine if loss of expression of two of the most commonly mutated tumour suppressors in endometrioid carcinoma, PTEN and ARID1A, was associated with increased proliferation in AH/EIN. We found that 80 (70%) of 114 cases exhibited decreased or undetectable PTEN and 17 (15%) of 114 cases had focal loss of ARID1A staining. ARID1A loss was focal, while PTEN loss was diffuse, and all specimens with ARID1A loss had concurrent PTEN loss (p = 0.0003). Mapping the distribution of PTEN and ARID1A staining in the same specimens demonstrated that all AH/EIN areas with ARID1A loss were geographically nested within the areas of PTEN loss. A significant increase in the proliferative activity was observed in areas of AH/EIN with concurrent loss of PTEN and ARID1A compared to immediately adjacent AH/EIN areas showing only PTEN loss. In a cell culture system, co-silencing of ARID1A and PTEN in human endometrial epithelial cells increased cellular proliferation to a greater degree than silencing either ARID1A or PTEN alone. These results suggest an essential gatekeeper role for ARID1A that prevents PTEN inactivation from promoting cellular proliferation in the transition of pre-cancerous lesions to uterine endometrioid carcinoma.

Indexed as

ARID1Aatypical hyperplasiaco‐silencingendometrioid intraepithelial neoplasiaimmunohistochemistryin vitro cell culture modelproliferationPTENtumour suppressor

Identifiers

PMID27499903
PMCPMC4939882
OpenAlexW1507577134

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.