Evidence map›Paper›PMID 31571090›Full record

ArticleInternational ophthalmology2020

CDKN2A, CDK1, and CCNE1 overexpression in sebaceous gland carcinoma of eyelid.

Tatsuya Yunoki, Tetsushi Hirano, Yoshiaki Tabuchi, Yukihiro Furusawa, Misako Torigoe, Takahiko Nakajima, Johji Imura, Atsushi Hayashi

Abstract read
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In one paragraph

Article in International ophthalmology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

3 citing papers in PubMed, 8 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 2 institutions in 1 country.

Tatsuya YunokiDepartment of Ophthalmology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan. yunokiki@med.u-toyama.ac.jp.ORCID http://orcid.org/0000-0003-3094-6406
Tetsushi HiranoDivision of Molecular Genetics Research, Life Science Research Center, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Yoshiaki TabuchiDivision of Molecular Genetics Research, Life Science Research Center, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Yukihiro FurusawaDepartment of Liberal Arts and Science, Toyama Prefectural University, 5180 Kurokawa, Toyama, 939-0398, Japan.
Misako TorigoeDepartment of Ophthalmology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Takahiko NakajimaDepartments of Diagnostic Pathology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Johji ImuraDepartments of Diagnostic Pathology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Atsushi HayashiDepartment of Ophthalmology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
University of Toyama · JPToyama Prefectural University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo investigate the overexpression of genes in sebaceous gland carcinoma (SGC) of the eyelid compared to sebaceous adenoma of the eyelid in order to elucidate the molecular mechanism underlying pathogenesis.

methodsWe performed histopathological examination of eyelid tissues surgically removed from four patients diagnosed with SGC (cases 1-3) and sebaceous adenoma (case 4) of the eyelid. Next, we performed global gene expression analysis of surgical tissue samples using a GeneChip

resultsIn the SGC samples, we found that 211, 199, and 199 genes, respectively, showed ≥ 2.0-fold higher expression than those in the sebaceous adenoma sample (case 4); 194 genes were common to all three SGC samples. For the 194 genes with upregulated expression, functional category analysis showed that SGC of the eyelid employed a unique gene network, including cyclin-dependent kinase inhibitor 2A (CDKN2A), cyclin-dependent kinase 1 (CDK1), and cyclin E1 (CCNE1), which are related to cell cycle progression, incidence of tumor, and cell viability. Furthermore, qRT-PCR analysis showed that the expression levels of CDKN2A, CDK1, and CCNE1 were significantly upregulated in all SGC cases compared to those in the sebaceous adenoma case. These data were similar to the results of microarray analysis.

conclusionOverexpression of cell cycle-related genes CDKN2A, CDK1, CCNE1, and their gene network may help elucidate the pathogenic pathway of SGC of the eyelid at the molecular level.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinoma, SebaceousAgedAged, 80 and overBiomarkers, TumorCDC2 Protein KinaseCyclin-Dependent Kinase Inhibitor p16Cyclin EEyelid NeoplasmsFemaleHumansImmunohistochemistryMaleOncogene ProteinsRNA, NeoplasmSebaceous Gland NeoplasmsBiomarkers, TumorCCNE1 protein, humanCDC2 Protein KinaseCDK1 protein, humanCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16Cyclin EOncogene ProteinsRNA, NeoplasmCyclin-dependent kinase 1Cyclin-dependent kinase inhibitor 2ACyclin E1Microarray analysisSebaceous gland carcinoma

Identifiers

PMID31571090
OpenAlexW2978450356

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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.