Evidence map›Paper›PMID 31828584›Full record

ArticleEndocrine pathology2020

A Novel Expression Profile of Cell Cycle and DNA Repair Proteins in Nonfunctioning Pituitary Adenomas.

Derya Metin-Armagan, Nil Comunoglu, Gulay Bulut, Pinar Kadioglu, Hiraku Kameda, Nurperi Gazioglu, Necmettin Tanriover, Melek Ozturk

Abstract read
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In one paragraph

Article in Endocrine pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-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

8 citing papers in PubMed, 10 citations in OpenAlex.

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  7. IncreasedDiagnostics (Basel, Switzerland) · 2020
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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 2 countries.

Derya Metin-ArmaganDepartment of Medical Biology, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul, Turkey.
Nil ComunogluDepartment of Pathology, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul, Turkey.
Gulay BulutDepartment of Molecular Biology and Genetics, Faculty of Engineering and Natural Sciences, Bahçeşehir University, Istanbul, Turkey.
Pinar KadiogluDepartment of Endocrinology and Metabolism, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Cerrahpasa, Istanbul, Turkey.
Hiraku KamedaDepartment of Rheumatology, Endocrinology and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Nurperi GaziogluDepartment of Neurosurgery, Istanbul Bilim University, Istanbul, Turkey.
Necmettin TanrioverDepartment of Neurosurgery, Cerrahpasa Medical School, Istanbul University- Cerrahpasa, Istanbul, Turkey.
Melek OzturkDepartment of Medical Biology, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul, Turkey. mozturk@istanbul.edu.tr.ORCID http://orcid.org/0000-0002-6227-1688
Istanbul University-Cerrahpaşa · TRBahçeşehir University · TRHokkaido University · JPIstanbul Bilim University · TR

Funding

Research Fund of the Istanbul University 2017-25404
6 · The paper itself

Abstract

The molecular mechanisms underlying the formation of nonfunctioning pituitary adenomas (NFAs) are largely unknown. In this study, we aimed to understand the relationship between NFAs and functional pituitary adenomas and the possible role of proteins involved in cell cycle, senescence, and DNA damage control mechanisms in the etiology of NFA. We analyzed pATM-S1981, pRb-S608, Rb, pE2F1-S364, p16, E2F1, p73, cyclin D1, and CHEK2 protein expression (in a group of 20 patients with acromegaly, 18 patients with Cushing's disease (CD), and 29 NFA patients) by immunohistochemistry and their relevant mRNA expression by qRT-PCR (in a group of 7 patients with acromegaly, 7 patients with CD, and 7 NFA patients). The clinical and histopathological results on the patients were statistically evaluated. pE2F1-S364 protein expression in the CD group was significantly lower than that in the NFA and acromegaly groups (p = 0.025, p = 0.034, respectively). However, the expression of the p16 protein was lower than in the NFA group than in the CD and acromegaly groups (p = 0.030, p = 0.033, respectively), and E2F1 protein expression was significantly higher in the NFA group than in the CD group (p = 0.025). p73 protein expression in patients with acromegaly was significantly higher (p = 0.031) than that in the CD group. CHEK2 mRNA expression in the CD group was significantly higher than that in the acromegaly group (p = 0.012). The selective and tumor-specific associations between E2F1, pE2F1-S364, CHEK2, and p73 mRNA and protein levels indicate their involvement in pituitary adenoma formation in NFA, CD, and acromegaly patients.

Indexed as

ACTH-Secreting Pituitary AdenomaAdenomaBiomarkers, TumorCell Cycle ProteinsDNA Repair EnzymesFemaleGrowth Hormone-Secreting Pituitary AdenomaHumansMalePituitary NeoplasmsRetrospective StudiesBiomarkers, TumorCell Cycle ProteinsDNA Repair EnzymesCHEK2E2F1Nonfunctioning pituitary adenomasp16p73pE2F1-S364RB

Identifiers

PMID31828584
OpenAlexW2995025293

What OpenQuestion holds

Textmetadata
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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.