Uncovering key genes and molecular mechanisms of dendritic cell dysfunction in Esophageal Cancer: implications for Novel Diagnostic and therapeutic strategies
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Le résumé fourni par la source
Dendritic cells play a crucial role in initiating and regulating immune responses, and their dysfunction is strongly associated with esophageal cancer. In this study, we aimed to develop a predictive signature and identify key genes linked to dendritic cell dysfunction in esophageal cancer. Through bioinformatics analysis of gene expression data from the TCGA database, we identified a set of 603 genes significantly associated with dendritic cell function. Further analysis using Cox regression and LASSO regression revealed six genes (GDF15, GPT, KRTAP5-5, MMP12, SLC5A1, and C5orf52) that were strongly correlated with overall survival. The prognostic signature constructed from these genes demonstrated that patients in the high-risk group had poorer survival outcomes compared to those in the low-risk group. Immune infiltration analysis indicated a higher abundance of macrophages in the high-risk group, and correlation studies showed a strong positive association between the risk score and the expression of immune checkpoint markers PD1 and PD-L1. Drug sensitivity analysis suggested that Metformin, Gefitinib, and Lapatinib may be more effective in the low-risk group, while Pyrimethamine, Axitinib, and Rapamycin may be more beneficial for high-risk patients. In summary, we identified a 6-gene signature related to dendritic cell dysfunction that can predict prognosis in esophageal cancer, offering valuable insights for personalized therapeutic strategies.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Uncovering key genes and molecular mechanisms of dendritic cell dysfunction in Esophageal Cancer: implications for Novel Diagnostic and therapeutic strategies
- Date Crossref
- 18/12/2024
- Éditeur
- Springer Science and Business Media LLC
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Les institutions déclarées
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