Evidence map›Paper›PMID 26033187›Full record

ArticleScientific reports2015

Urokinase-type plasminogen activator resulting from endometrial carcinogenesis enhances tumor invasion and correlates with poor outcome of endometrial carcinoma patients.

Chia-Yen Huang, Ming-Cheng Chang, Wei-Yun Huang, Ching-Ting Huang, Yu-Chien Tang, Hsien-Da Huang, Kuan-Ting Kuo, Chi-An Chen, Wen-Fang Cheng

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. 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
1.0field-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

8 citing papers in PubMed, 12 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

9 authors at 3 institutions in 1 country.

Chia-Yen Huang1] Gynecologic Cancer Center, Department of Obstetrics and Gynecology, Cathay General Hospital, Taipei, Taiwan [2] Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Ming-Cheng ChangDepartment of Obstetrics and Gynecology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Wei-Yun HuangDepartment of Biological Science and Technology, Institute of Bioinformatics and Systems Biology, National Chiao Tung University, Hsin-Chu, Taiwan.
Ching-Ting HuangGraduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Yu-Chien TangDepartment of Obstetrics and Gynecology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Hsien-Da HuangDepartment of Biological Science and Technology, Institute of Bioinformatics and Systems Biology, National Chiao Tung University, Hsin-Chu, Taiwan.
Kuan-Ting KuoDepartment of Pathology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Chi-An ChenDepartment of Obstetrics and Gynecology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Wen-Fang Cheng1] Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan [2] Department of Biological Science and Technology, Institute of Bioinformatics and Systems Biology, National Chiao Tung University, Hsin-Chu, Taiwan [3] Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan.
National Taiwan University · TWNational Yang Ming Chiao Tung University · TWCathay General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purpose of this study was to identify the dysregulated genes involved in the tumorigenesis and progression of endometrial endometrioid adenocarcinoma (EEC), and their possible mechanisms. Endometrial specimens including normal endometrial tissues, atypical endometrial hyperplasia, and EEC were analyzed. The expression profiles were compared using GeneChip Array. The gene expression levels were determined by real-time RT-PCR in the training and testing sets to correlate the clinico-pathological parameters of EEC. Immunoblotting, in vitro cell migration and invasion assays were performed in human endometrial cancer cell lines and their transfectants. In microarray analysis, seven dysregulated genes were identified. Only the levels of urokinase-type plasminogen activator (uPA) were higher in EEC with deep myometrial invasion, positive lympho-vascular space invasion, lymph node metastasis, and advanced stages. After multivariate analysis, uPA was the only independent poor prognostic factor for disease-free survival in the EEC patients (hazard ratio: 4.65, p = 0.03). uPA may enhance the migratory and invasive capabilities of endometrial tumor cells by the phosphorylation of ERK1/2, Akt and p38 molecules. uPA is a dysregulated gene involved in the tumorigenesis, bio-pathological features and outcomes of EEC. uPA may be a potential molecule and target for the detection and treatment of EEC.

Indexed as

AdultAgedCell Line, TumorCell MovementCell Transformation, NeoplasticCluster AnalysisEndometrial NeoplasmsFemaleGene Expression ProfilingHumansMAP Kinase Signaling SystemMiddle AgedNeoplasm GradingNeoplasm InvasivenessNeoplasm MetastasisNeoplasm Stagingp38 Mitogen-Activated Protein KinasesPLOD2 protein, humanProcollagen-Lysine, 2-Oxoglutarate 5-DioxygenaseProto-Oncogene Proteins c-aktRNA, MessengerUrokinase-Type Plasminogen Activator

Identifiers

PMID26033187
PMCPMC4451531
OpenAlexW1041812087

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.