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Relationship between Monoclonal Gammopathy of undetermined significance and multiple myeloma via online database analysis

OBJECTIVE: To explore the relationship between Monoclonal Gammopathy of undetermined significance (MGUS) and Multiple Myeloma (MM) based on bioinformatics methods. METHODS: In this study, we conducted bioinformatics to identify genes associated with MGUS and MM using the PubMed pubmed2ensemble (http...

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Detalles Bibliográficos
Autores principales: Lu, Weiguo, Liu, Jiaming, Luo, Man, Xiao, Mingfeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Professional Medical Publications 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10214783/
https://www.ncbi.nlm.nih.gov/pubmed/37250588
http://dx.doi.org/10.12669/pjms.39.3.7206
Descripción
Sumario:OBJECTIVE: To explore the relationship between Monoclonal Gammopathy of undetermined significance (MGUS) and Multiple Myeloma (MM) based on bioinformatics methods. METHODS: In this study, we conducted bioinformatics to identify genes associated with MGUS and MM using the PubMed pubmed2ensemble (http://pubmed2ensembl.ls.manchester. ac.uk/) until 2021. Gene ontology function was used to label overlapping genes, and Kyoto Encyclopedia of Genes and Genomes analysis was used to identify enriched pathways. The cluster-1 genes obtained from Cytoscape were analyzed by Comparative Toxicogenomics Database (CTD, http://ctdbase.org/) and then used to screen candidate drugs using the DSigDB database (https://amp.pharm.mssm.edu/Enrichr/). RESULTS: In total, 227 genes were common to both MGUS and MM. These genes were significantly associated with cytokine-cytokine receptor interaction and the PI3K-Akt signaling pathway. The protein-protein interaction network revealed that TNF, IL-1B, IL-6, CSF2, CXCL8, and IL-10 were among the core genes of MM. Finally, eight candidate drugs showed maximum interaction with core genes, which could potentially prevent MGUS from progressing to MM. CONCLUSION: The progression of MGUS to MM is driven by aberrant cytokine secretion, which leads to inflammation immune dysfunction, and dysregulation of the PI3K/AKT/mTOR signaling pathway.