ArticleFrontiers in immunology2025
Multi-omics analysis reveals glutathione metabolism-related immune suppression and constructs a prognostic model in lung adenocarcinoma.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- A Rho GTPase-related gene signature predicts prognosis and reveals an immunosuppressive microenvironment in lung adenocarcinoma: an integrated analysis of bulk and single-cell RNA sequencing data.Scientific reports · 2026Article
- The Glutamate-Glutathione axis in neuropsychiatric disorders and cancer: From shared mechanisms to non-invasive biomarkers.Redox biology · 2026Review
- PYCR1 promotes glutamine metabolism and the progression of lung adenocarcinoma by regulating the expression of OPLAH.Clinical and experimental medicine · 2026Article
- A Pan-Cancer Transcriptomic Signature for Conserved Molecular Programs Underlying Premalignant-Malignant Progression Across Common Carcinomas.Dentistry journal · 2026Article
- Mendelian randomization analysis reveals causal associations between HLA gene expression, inflammatory biomarkers, and non-small cell lung cancer risk.Discover oncology · 2026Article
- A Glutathione Metabolism-Related Transcriptomic Signature for Prognostic Assessment and Biological Characterization of Lung Adenocarcinoma.Cancer informatics · 2026Article
- Development of a lipoprotein(a)-based model for predicting progression-free survival and grade3/4 adverse events in driver gene negative metastatic lung adenocarcinoma patients with PD-L1 TPS <50.Frontiers in immunology · 2026Article
- Interpretable machine learning model integrating CT radiomics, CTR, and clinical features for EGFR mutation prediction in ≤3 cm lung adenocarcinoma nodules.Annals of medicine · 2025Article
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Authors and funding
6 authors.
Funding
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Abstract
Background: Metabolic reprogramming within the tumor microenvironment plays a pivotal role in tumor progression and therapeutic responses. Nevertheless, the relationship between aberrant glutathione (GSH) metabolism and the immune microenvironment in lung adenocarcinoma, as well as its clinical implications, remains unclear. Methods: We leveraged genome-wide association study (GWAS) data and applied genetic causal analysis to evaluate the causal relationships among plasma 5-oxoproline levels, lung adenocarcinoma (LUAD) risk, and 731 immune phenotypes. We incorporated single-cell RNA sequencing data from LUAD to compare transcription factor activity, cell communication networks, and CD8 Results: Genetic causal analysis indicated a positive correlation between plasma 5-oxoproline levels and LUAD risk. ScRNA-seq analysis revealed an increased proportion of exhausted CD8 Conclusions: GSH metabolic reprogramming may suppress antitumor immunity by modulating transcription factor activity, remodeling cell communication networks, and regulating CD8+ T cells. The prognostic risk model developed herein effectively predicts immunotherapeutic response, drug sensitivity, and overall survival in patients with LUAD.
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