TNFRSF18 (TNF Receptor Superfamily Member 18)

This study offers a comprehensive landscape of immune cell proportions within the cervical cancer TME and uncovers a complexity in the relationships between gene expression and tumour-infiltrating immune cell subsets. These results will provide valuable clues for the study of the immune microenvironment in cervical cancer and will shed some light into novel therapeutic approaches.

Our investigation comprehensively characterized the cellular diversity and molecular features of the cervical cancer microenvironments.

In vitro, the system effectively inhibited ccRCC cell proliferation and downregulated TNFRSF18, a key immunomodulatory gene. This study provides a redox-responsive, fluorescence-trackable delivery platform for everolimus, offering potential for targeted and immune-synergistic therapy in ccRCC.

Our findings establish SPP1+TNFRSF18+ CD4+ T cells as central regulators of HCC immune suppression, offering novel strategies to enhance HCC immunotherapy.

High-risk patients showed poorer overall survival (OS), distinct immune cell infiltration, elevated expression of KIR2DL1, LGALS9, TNFRSF18, and TNFRSF4, increased sensitivity to imatinib and axitinib, resistance to multiple chemotherapeutics, and reduced Fusobacteria and Tenericutes abundance. HAAO, ALDH2, and lymph node stage were identified as independent prognostic factors and were used to develop a predictive nomogram. We identified a Trp metabolism-associated fibroblast population in the ESCC tumor microenvironment (TME) and developed a five-gene TrpG signature for prognostic prediction in ESCC patients.

  Multi-omics analysis reveals dynamic CD8+ T cell exhaustion patterns across CRC samples with different TNM stages. TNFRSF18 is highly expressed in exhausted tumour-infiltrating CD8+ T cells and declines with disease progression. Ribosomal stemness in tumour cells promotes immune evasion by impairing TNF-mediated CD8+ T cell function.

Notably, CD7, CXCL6, FASN, FLT3LG, LTB, and TNFRSF18 were significantly downregulated, marking a potential transcriptomic signature of systemic immune impairment. These findings suggest that immune dysfunction in the PI group is not solely attributable to conventional immune suppression but rather to a diminished immune activation state driven by reduced TNFRSF gene expression.

These four immunomodulatory genes were used to construct a prognostic model for gastric cancer.Gastric cancer patients with high CTHRC1 expression have a poor prognosis and are associated with immune cell infiltration. Therefore, CTHRC1 can be considered as a potentially reliable prognostic indicator for gastric cancer patients.

ADM held promise as a prognostic biomarker and a potential therapeutic target in immune modulation and resistance management. Future research should focus on experimental validation and elucidation of ADM-mediated pathways, which might provide novel insights into cancer biology and improve clinical outcomes.

Finally, the expression of BTG2, TANK, and EIF4E3 was verified by RT-PCR, which was consistent with the bioinformatics analysis. The 7 prognostic genes (PGK1, BTG2, TANK, CFB, EIF4E3, TNFRSF18, and BATF) were screened, providing new insights into potential treatments for BRCA.

Furthermore, nine candidate drugs with potential therapeutic efficacy in EC were identified: Bleomycin, Cisplatin, Cyclopamine, PLX4720, Erlotinib, Gefitinib, RO.3306, XMD8.85, and WH.4.023. Furthermore, it identifies potential therapeutic agents with efficacy against EC. These findings hold significant promise for enhancing the survival of EC patients and provide valuable insights to inform clinical decision-making in the management of this disease.

The TME, three DEGs and Risk Score can effectively serve as biomarkers to elucidate the immune landscape and predict prognosis in LUSC patients. They may provide insights to the investigations on therapeutic strategies for LUSC.