PTGDS (Prostaglandin D2 Synthase)

Furthermore, Meflin deficiency reduced the area of tumor vessels in a TNBC mouse model, highlighting its role in CAF-mediated inhibition of TNBC progression and improvement of drug delivery. Accordingly, Meflin plays a role as a potential functional marker of rCAFs in TNBC.

This study identifies glycosylation-related gene candidates and establishes a preliminary diagnostic model for SLE, utilizing integrated bioinformatics analysis and experimental validation. These findings provide foundational insights for further exploration of SLE's molecular mechanisms and diagnostic advancement.

Elevated expression of PTGDS was observed in hiPSC-CMs treated with the pro-hypertrophic cytokine leukemia inhibitory factor (LIF) and in end-stage heart failure patients, ascertaining its importance in cardiac disease settings. PTGDS is a newly identified mediator of Aldo-MR-induced cardiac remodeling and may represent a potential therapeutic target for CVD.

Combining it with anti-PD-L1 improves BRCA treatment. PTGDS is a potential prognostic biomarker and a novel immunotherapy target for BRCA.

Notably, the TLS_H group demonstrated enhanced sensitivity to chemotherapeutics including AZD8055, axitinib, vorinostat, nilotinib, camptothecin and paclitaxel. Real-time fluorescent quantitative PCR (RT-qPCR) validation in Mia PaCa2 and Jurkat cells indicated that LAT, RBP5 and SKAP1 may play important roles in modulating sensitivity to these chemotherapeutics. These findings establish TLS as a potential biomarker for PAAD, enabling personalised chemotherapy selection by integrating immune contexture and genomic drivers to improve clinical outcomes.

PTGDS deficiency promotes immunosuppressive TME remodeling and predicts unfavorable clinical outcomes in ESCC, which might be a potential prognostic biomarker in ESCC.

These findings were further supported by RT-qPCR and immunofluorescence data, which confirmed the downregulation of PTGDS and PTGDR in LUAD tumor tissues compared to normal tissues. Collectively, these results suggest that PGD2 and its signaling axis play a significant role in tumor-suppressive and anti-inflammatory effects in LUAD, with potential applications in prognosis management and therapy decision-making.

Our study provides a comprehensive comparison of AM and MM, uncovering subtype-specific stromal-immune interactions and molecular programs. The findings highlight actionable targets (e.g., TIGIT in AM, CXCL3⁺ macrophages in MM) and propose a framework for precision therapies, biomarker-driven trials, and risk stratification to improve outcomes in these aggressive melanomas.

QRT-PCR detection of Clinical LUAD samples also validated the differentially expression of CDIGPM model related genes.ConclusionsThe study highlights the prognostic importance of CDIGs in LUAD using the CDIGPM model, linking age, stage and CDIGPM score to poor outcomes. The identified genes and pathways provide potential therapeutic targets, deepening our understanding of LUAD's molecular landscape.

Taken together, our findings firstly identified that targeting PTGDS promotes the ferroptosis in PTCL through regulating HMOX1-mediated iron metabolism, and highlighted novel therapeutic strategies to improve the efficacy of ferroptosis-targeted therapy in PTCL patients.