Evidence map›Paper›PMID 32599983›Full record

ArticleCancer research and treatment2020

FGFR4 Gly388Arg Polymorphism Affects the Progression of Gastric Cancer by Activating STAT3 Pathway to Induce Epithelial to Mesenchymal Transition.

Yanwei Ye, Jie Li, Dongbao Jiang, Jingjing Li, Chuangfeng Xiao, Yingze Li, Chao Han, Chunlin Zhao

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer research and treatment, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 43% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Frontiers in oncology · 2021
    Pooled it
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  5. Review
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 3 institutions in 1 country.

Yanwei YeDepartment of Gastrointestinal Surgery and Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jie LiDepartment of General Surgery, Tongchuan People's Hospital, Shanxi, China.
Dongbao JiangDepartment of Thyroid, and Breast Surgery, Xinxiang Central Hospital, Xinxiang, China.
Jingjing LiDepartment of Infectious Disease, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Chuangfeng XiaoDepartment of Gastrointestinal Surgery and Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yingze LiDepartment of Gastrointestinal Surgery and Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Chao HanDepartment of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Chunlin ZhaoDepartment of Gastrointestinal Surgery and Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
First Affiliated Hospital of Zhengzhou University · CNThe People's Hospital Tongling · CNXinxiang Central Hospital · CN

Funding

Foundation of Henan Educational Committee 19A320080Zhengzhou University and National Natural Science Foundation of China 81201955
6 · The paper itself

Abstract

purposeFibroblast growth factor receptor 4 (FGFR4) plays a critical role in cancer progression involving in tumor proliferation, invasion, and metastasis. This study clarified the role of FGFR4-Arg388 variant in gastric cancer (GC), and more importantly highlighted the possibility of this single nucleotide polymorphism (SNP) as potential therapeutic targets. MATERIALS AND

methodsFGFR4 polymorphism was characterized in advanced GC patients to perform statistical analysis. FGFR4-dependent signal pathways involving cell proliferation, invasion, migration, and resistance to oxaliplatin (OXA) in accordance with the SNP were also assessed in transfected GC cell lines.

resultsAmong 102 GC patients, the FGFR4-Arg388 patients showed significantly higher tumor stage (p=0.047) and worse overall survival (p=0.033) than the Gly388 patients. Immunohistochemical results showed that FGFR4-Arg388 patients were more likely to have higher vimentin (p=0.025) and p-STAT3 (p=0.009) expression compared with FGFR4-Gly388 patients. In transfected GC cells, the overexpression of FGFR4-Arg388 variant increased proliferation and invasion of GC cells, increasing resistance of GC cells to OXA compared with cells overexpressing the Gly388 allele.

conclusionThe exploration mechanism may be through FGFR4-Arg388/STAT3/epithelial to mesenchymal transition axis regulating pivotal oncogenic properties of GC cells. The FGFR4-Arg388 variant may be a biomarker and a candidate target for adjuvant treatment of GC.

Indexed as

Antineoplastic AgentsBiomarkers, TumorCell Line, TumorChemotherapy, AdjuvantDisease ProgressionDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleGastrectomyHumansKaplan-Meier EstimateMaleNeoplasm StagingOxaliplatinPolymorphism, Single NucleotidePrognosisAntineoplastic AgentsBiomarkers, TumorFGFR4 protein, humanOxaliplatinReceptor, Fibroblast Growth Factor, Type 4STAT3 protein, humanSTAT3 Transcription FactorEpithelial to mesenchymal transitionFibroblast growth factor receptor 4Gastric neoplasmsGly388Arg polymorphismSTAT3

Identifiers

PMID32599983
PMCPMC7577822
OpenAlexW3026331063

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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.