Evidence map›Paper›PMID 28640074›Full record

ArticleMedicine2017

Bioinformatics analysis of key genes and pathways for hepatocellular carcinoma transformed from cirrhosis.

Bosheng He, Jianbing Yin, Shenchu Gong, Jinhua Gu, Jing Xiao, Weixiang Shi, Wenbin Ding, Ying He

Open access · goldAbstract read
In one paragraph

Article in Medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

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  13. Identification of Time-Invariant Biomarkers for Non-Genotoxic Hepatocarcinogen Assessment.International journal of environmental research and public health · 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 3 institutions in 1 country.

Bosheng HeDepartment of Radiology, the Second Affiliated Hospital of Nantong University Department of Pathophysiology, Nantong University Medical School Department of Epidemiology and Medical Statistics, School of Public Health, Nantong University Department of Ultrasound, the Tumor Hospital of Nantong University, Nantong, Jiangsu, China.
Jianbing Yin
Shenchu Gong
Jinhua Gu
Jing Xiao
Weixiang Shi
Wenbin Ding
Ying He
Affiliated Hospital of Nantong University · CNNantong University · CNSecond Affiliated Hospital of Nantong University

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveWe aimed to identify some pivotal genes and pathways for hepatocellular carcinoma (HCC) transformation from cirrhosis and explore potential targets for treatment of the disease.

methodsThe GSE17548 microarray data were downloaded from Gene Expression Omnibus database, and 37 samples (20 cirrhosis and 17 HCC samples) were used for analysis. The differentially expressed genes (DEGs) in HCC tissues were compared with those in cirrhosis tissues and analyzed using the limma package. Gene ontology-biological process and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analyses were performed using ClueGO and CluePedia tool kits, and the key KEGG pathway was analyzed using the R package pathview. The regulatory factor miRNA of DEGs was extracted from 3 verified miRNAs-target databases using the multiMiR R package. Moreover, a protein-protein interaction (PPI) network was constructed using the Cytoscape software.

resultsDEGs including cyclin-dependent Kinase 1 (CDK1), PDZ-binding kinase (PBK), ribonucleotide reductase M2 (RRM2), and abnormal spindle homolog, and microcephaly-associated drosophila (ASPM) were the hub proteins with higher degrees in the PPI network. The cell cycle pathway (CDK1 enriched) and p53 signaling pathway (CDK1 and RRM2 enriched) were significantly enriched by DEGs.

conclusionCDK1, PBK, RRM2, and ASPM may be key genes for HCC transformation from cirrhosis. Furthermore, cell cycle and p53 signaling pathways may play vital mediatory roles; CDK1 may play crucial roles in HCC transformed from cirrhosis via cell cycle and p53 signaling pathways, and RRM2 might be involved in HCC transformed from cirrhosis via the p53 signaling pathway.

Indexed as

AdultAgedCarcinoma, HepatocellularCDC2 Protein KinaseComputational BiologyDisease ProgressionFemaleGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseHumansLiverLiver CirrhosisLiver NeoplasmsMaleMicroarray AnalysisMicroRNAsASPM protein, humanCDC2 Protein KinaseMicroRNAsMitogen-Activated Protein Kinase KinasesNerve Tissue ProteinsPDZ-binding kinaseRibonucleoside Diphosphate Reductaseribonucleotide reductase M2Tumor Suppressor Protein p53

Identifiers

PMID28640074
PMCPMC5484182
OpenAlexW2717429551

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.