AI Article Synopsis

  • WHO Grade 2/3 gliomas are common brain tumors that significantly impact patients' quality of life and survival, with recent research highlighting the importance of the TCA cycle and a new programmed cell death mechanism called cuproptosis in their development.
  • Eight out of ten identified cuproptosis-related genes (CRGs) show different expression levels in normal versus glioma tissues, leading to the development of risk signatures that can predict patient prognosis and are linked to clinical features.
  • Key independent risk factors like FDX1 and CDKN2A have been identified as potential prognostic biomarkers for WHO 2/3 glioma, providing a promising avenue for improved diagnosis and treatment strategies.

Article Abstract

WHO 2/3 glioma is a common intracranial tumor that seriously affects the quality of life and survival time of patients. Previous studies have shown that the tricarboxylic acid (TCA) cycle is closely related to the occurrence and development of glioma, while recent studies have shown that cuproptosis, a novel programmed death pathway, is closely related to the inhibition of the TCA cycle. In our study, eight of ten cuproptosis-related genes (CRGs) were found to be differentially expressed between normal and WHO 2/3 glioma tissues. Through the LASSO algorithm, the cuproptosis-associated risk signatures (CARSs) were constructed, which can effectively predict the prognosis of WHO 2/3 glioma patients and are closely related to clinicopathological features. We analyzed the relationship between risk score and immune cell infiltration through Xcell, ssGSEA, TIMER database, and immune checkpoint molecules. In addition, the relationship between risk score and chemotherapeutic drug sensitivity was also investigated. The prognosis-related independent risk factors FDX1 and CDKN2A identified from CARSs are considered potential prognostic biomarkers for WHO 2/3 glioma. The clinical prognosis model based on cuproptosis is expected to provide an effective reference for the diagnosis and treatment of clinical WHO 2/3 glioma patients.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9434124PMC
http://dx.doi.org/10.3389/fonc.2022.967159DOI Listing

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