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http://purl.uniprot.org/citations/35183683http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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Background

Glioma is one of the most prevalent malignant brain tumors and its incidence is rising continuously in recent years. Studies suggested that the regulatory mechanism of CDK2 in glioma might different from most of the other cancer types METHODS: Data were accessed from TCGA, GTEx, CGGA, CancerSEA, and TISCH. The expressions of CDK2 in tumors, normal tissues, and different groups of gliomas were compared. The association between CDK2 and the overall survival of glioma patients was analyzed and validated, and a prognostic model was constructed. CDK2-associated genes were enriched in the GO and the KEGG pathways. The association of CDK2 and tumor immunity and functions were analyzed. The subtypes of glioma cells expressing CDK2 were identified.

Results

CDK2 was overexpressed in glioma compared to normal brain tissues. CDK2 was overexpressed in higher grade glioma compared to lower grade glioma. CDK2 expression was higher in groups related to poor prognostic factors in low-grade glioma but had no difference in high-grade glioma. CDK2 was associated with worse overall survival in overall glioma and within low-grade glioma. A survival prediction nomogram was constructed. The enrichment study revealed that the low expression of CDK2 was associated with genes regulating normal brain functions while the high expression of CDK2 was associated with genes regulating immune cells and cancer. CDK2 was negatively correlated with B cells, T cells CD4+, and T cells CD8+. CDK2 was positively correlated with endothelial cells, macrophage, and NK cells. CDK2 high group had higher expression of the immune checkpoint genes, and the calculation suggested that patients with a lower CDK2 expression were much more likely to respond to immunotherapy.

Conclusion

CDK2 was a potential diagnostic and prognostic biomarker and novel tumor immune environment sign for glioma patients."xsd:string
http://purl.uniprot.org/citations/35183683http://purl.org/dc/terms/identifier"doi:10.1016/j.gene.2022.146325"xsd:string
http://purl.uniprot.org/citations/35183683http://purl.uniprot.org/core/author"Liu H."xsd:string
http://purl.uniprot.org/citations/35183683http://purl.uniprot.org/core/author"Weng J."xsd:string
http://purl.uniprot.org/citations/35183683http://purl.uniprot.org/core/date"2022"xsd:gYear
http://purl.uniprot.org/citations/35183683http://purl.uniprot.org/core/name"Gene"xsd:string
http://purl.uniprot.org/citations/35183683http://purl.uniprot.org/core/pages"146325"xsd:string
http://purl.uniprot.org/citations/35183683http://purl.uniprot.org/core/title"A comprehensive bioinformatic analysis of cyclin-dependent kinase 2 (CDK2) in glioma."xsd:string
http://purl.uniprot.org/citations/35183683http://purl.uniprot.org/core/volume"822"xsd:string
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