GPRC5A (G Protein-Coupled Receptor Class C Group 5 Member A)

Therapeutically, HSP90 inhibition synergizes with anti-PD1 in inflammatory iCCA, whereas combined anti-PD1 and anti-TIM3 suppresses neurodegenerative iCCA. Collectively, our study provides a robust molecular framework and actionable therapeutic strategies for iCCA.

Our results identify TICs as the origin of neoplastic stem‑like states in the conventional tubular adenoma pathway and define early transcriptional, metabolic, and microenvironmental reprogramming events that distinguish TICs from nSTMs. In contrast to serrated pathways described in other atlases, our data support a stem‑like expansion model for tubular adenomas and nominate biomarkers with translational potential for early CRC detection and intervention.

The Hippo pathway represents a critical yet underappreciated dimension of ccRCC biology, offering promising biomarkers for risk stratification and novel therapeutic targets. The Hippo-VHL nexus presents multiple intervention points that could enhance current treatment.

Integrating single-cell and bulk transcriptomes links malignant epithelial state programs to prognosis, yields a practical eight-gene risk model validated in multiple LUAD cohorts, and nominates FAM189A2 as a putative tumor suppressor and potential biomarker in lung cancer. These findings suggest testable strategies for risk stratification and therapy selection that warrant prospective evaluation.

Our findings indicated that the rondom froest model based on five autoantibodies might help identify preclinical and early-stage PC.

Furthermore, NK92 cell-derived exosomes effectively delivered ABCB1 siRNA into recipient cells, mediating efficient gene silencing to sensitize chemoresistant ovarian cancer cells to therapeutic agents. Overall, this study provides a novel strategy to treat ovarian cancer through the preparation of genetically modified NK92 cell-derived exosomes loaded with RNA interference.

Conclusions : This study identifies TICs as the developmental origin of neoplastic stem-like states and delineates early transcriptional and pathway reprogramming events that drive the transition from normal to premalignant colonic epithelium. These findings provide new insight into CRC initiation and nominate biomarkers with translational potential for early detection and therapeutic targeting.

This study provides new insights into the endocytic mechanisms of GPRC5A, for which no specific ligand has been identified to date. Further research may uncover additional Gal-3-mediated functions in GPRC5A cellular signaling and contribute to the development of innovative therapeutic strategies.

These findings were confirmed using primary CAFs and NFs models. Our study unveils GPRC5A as a key mediator in ESCC and proposes the GPRC5A/TGF-β/ANXA1 axis as a promising therapeutic target for ESCC treatment.

This study highlights the potential of GPD2 and the glycolysis-related gene signature as prognostic biomarkers and therapeutic targets in CCA. The signature offers insights into tumor biology, immune interactions, and potential personalized treatment strategies, paving the way for improved management of this aggressive cancer.

An interactive web portal to explore the full results and visualizations is available at pc-biomarkers.de. Future work will further validate these biomarkers to improve early detection, prognosis, and treatment strategies.

This study proposes a glycolysis assessment strategy based on the interquartile range, which effectively addresses the limitations of previous scoring methods, including insufficient resolution and limited robustness. The proposed method enables more accurate quantification of intracellular glycolysis levels and facilitates fine-grained characterization of metabolic states. Furthermore, it identifies GPRC5A as a potential biomarker for the early diagnosis of gastric cancer. These findings enhance our understanding of metabolic reprogramming in gastric cancer and provide support for targeting the glycolytic pathway in therapeutic interventions.