PTGER4 (Prostaglandin E Receptor 4)

These findings suggest PTGER4 plays a central role in KIRC progression and treatment response. Targeting RiboSis-related mechanisms and PTGER4-related pathways could lead to better therapies for KIRC patients.

Mechanistically, PTGER4 expression correlated with multiple immune checkpoints. In mouse models, PTGER4 overexpression enhanced the efficacy of PD-1 blockade by promoting CD8⁺ T cell infiltration and function, as indicated by increased levels of IFN-γand Granzyme B. This study establishes a TME-centric prognostic framework, revealing that while the composite TCR-IRG score generally indicates a higher risk of tumor progression, individual components like PTGER4 may paradoxically mark a T-cell state amenable to reinvigoration by immunotherapy, highlighting the context-dependent utility of immune biomarkers in oncology.

EP4 plays a significant role in modulating bortezomib resistance in multiple myeloma through its effects on the PI3K/AKT pathway and ER stress. These findings underscore the therapeutic potential of targeting EP4 to enhance bortezomib efficacy and improve clinical outcomes for patients with multiple myeloma.

In summary, PGE2-induced N2-type TAN polarization directly affects the malignant progression of tumors. Our research revealed that PGE2 could be a potential effective molecule for targeting TANs in antitumor immunotherapy for CRC.

This study demonstrates combining imaging with cfDNA methylation and 7-AABs enhances preoperative risk stratification. These biomarkers also show promise for evaluating treatment response and guiding surveillance, supporting their use in precise lung cancer management.

The accuracy of the model was significantly higher than the individual biomarkers. These results demonstrated that this panel based on four methylation markers and cfDNA concentration was effective in lung cancer detection, and may provide clinical utility in combination with current lung cancer detection techniques to improve the diagnosis of lung cancer.

Glycosylated flavonols, anthocyanidins, flavones, and coumarins showed strong predicted interactions with key inflammatory targets (ALOX15, ALOX5, PTGER4, and NOS2) and metabolic regulators (GSK3A and PI4KB), providing mechanistic support for observed therapeutic effects and suggesting potential applications in chronic inflammatory and metabolic diseases. These findings underscore the substantial therapeutic potential of underexplored Pelargonium species and advocate for systematic research employing untargeted metabolomics, standardized bioassays, and compound-specific mechanistic validation to fully unlock the pharmacological potential of this diverse genus.

High EP4 receptor expression suggests inflammation may play a role in the development of feline HNSCC. Therapeutically targeting the EP4 receptor with antagonists may add to the current treatment options for this devastating cancer.

After 30 days of initial treatment, peripheral blood gene methylation levels decreased significantly. In conclusion, the combined detection of peripheral blood gene methylation can identify high-risk acute leukemia patients, serve as a prognostic marker, and be used for post-treatment follow-up monitoring.

These findings suggest that SHOX2, RASSF1A, and PTGER4 gene methylation could be valuable biomarkers for the early detection of LC, particularly in high-risk populations or those with atypical presentations. However, further studies with larger sample sizes and longitudinal designs are needed to confirm these findings and evaluate the long-term clinical utility of these methylation markers in monitoring disease progression and treatment response.

High PTGER2 expression was significantly associated with worse prognosis in patients with high CD8 expression. These insights advance our understanding of H. pylori's influence on T cell responses in gastric cancer, aiding in treatment and prognostic strategies.

Interestingly, CSF1R expression was significantly enriched in C1QC + macrophages versus SPP1 + macrophages, possibly explaining limited anti-CSF1R monotherapy effects. In conclusion, we propose an SPP1 + macrophage model in CRC, highlighting such macrophages as a promising therapeutic target due to their malignancy markers.