Evidence map›Paper›PMID 33575336›Full record

ArticleBioMed research international2021

Potential Drug Prediction of Glioblastoma Based on Drug Perturbation-Induced Gene Expression Signatures.

Bochi Zhu, Xijing Mao, Yuhong Man

RetractedAbstract readRetracted Publication
In one paragraph

Article in BioMed research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

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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

2 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Bochi ZhuDepartment of Neurology, The Second Hospital of Jilin University, Changchun City, Jilin Province, 130041, China.
Xijing MaoDepartment of Neurology, The Second Hospital of Jilin University, Changchun City, Jilin Province, 130041, China.
Yuhong ManDepartment of Neurology, The Second Hospital of Jilin University, Changchun City, Jilin Province, 130041, China.ORCID https://orcid.org/0000-0002-4253-1446

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesGlioblastoma (GBM) is a malignant brain tumor which is the most common and aggressive type of central nervous system cancer, with high morbidity and mortality. Despite lots of systematic studies on the molecular mechanism of glioblastoma, the pathogenesis is still unclear, and effective therapies are relatively rare with surgical resection as the frequently therapeutic intervention. Identification of fundamental molecules and gene networks associated with initiation is critical in glioblastoma drug discovery. In this study, an approach for the prediction of potential drug was developed based on perturbation-induced gene expression signatures.

methodsWe first collected RNA-seq data of 12 pairs of glioblastoma samples and adjacent normal samples from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified by DESeq2, and coexpression networks were analyzed with weighted gene correlation network analysis (WGCNA). Furthermore, key driver genes were detected based on the differentially expressed genes and potential chemotherapeutic drugs and targeted drugs were found by correlating the gene expression profiles with drug perturbation database. Finally, RNA-seq data of glioblastoma from The Cancer Genome Atlas (TCGA) dataset was collected as an independent validation dataset to verify our findings.

resultsWe identified 1771 significantly DEGs with 446 upregulated genes and 1325 downregulated genes. A total of 24 key drivers were found in the upregulated gene set, and 81 key drivers were found in the downregulated gene set. We screened the Crowd Extracted Expression of Differential Signatures (CREEDS) database to identify drug perturbations that could reverse the key factors of glioblastoma, and a total of 354 drugs were obtained with

conclusionsIn this study, we provided a framework of workflow for potential therapeutic drug discovery and predicted 10 potential drugs for glioblastoma therapy.

Indexed as

Brain NeoplasmsGlioblastomaAntineoplastic AgentsDatabases, GeneticDrug DiscoveryGene Expression ProfilingGene Expression Regulation, NeoplasticHumansTranscriptomeAntineoplastic Agents

Identifiers

PMID33575336
PMCPMC7857867

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