CTSD (Cathepsin D)

The CSTD simulation reduced 114 vials but resulted in a 2.76% increase in total cost (R$ 125,789.92 vs. R$ 122,416.55). An increase in treated patients (256 vs. 245) and completed cycles (1118 vs. 1074) was observed.ConclusionAlthough direct cost reduction was not achieved, CSTD use may eliminate waste, expand patient access, and optimize public healthcare resources.

The results of this research provide value to the field of proteomics as a large-scale, reproducible, and hypothesis-generating plasma dual-omics reference dataset. This study was not designed to establish diagnostic biomarkers, to assess clinical discriminative performance, or to imply causal mechanisms. Instead, by emphasizing reproduciblilty across independent cohorts, we provide a plasma dual-omics reference dataset that captures coordinated immune and lipid metabolic alterations associated with chronic liver disease severity. These data provide a framework and resource for future studies researching risk stratification, therapeutic monitoring, and mechanistic validation in chronic liver disease.

In parallel, IFN-β activates STAT1/STAT3 to upregulate cathepsin D expression, whereas TGF-β enhances GSDME phosphorylation by downregulating PPP1R3G, a regulatory subunit of protein phosphatase 1. Using lipid-hybrid nanoparticle-delivered mRNA technology, the tri-cytokine cocktail demonstrated therapeutic efficacy against orthotopic PDAC in mice and PDX models, highlighting its translational potential for PDAC patients.

Our study offers a foundational framework for using PGRN in glioma diagnosis and prognosis. The potential of PGRN as both a diagnostic and prognostic biomarker was identified suggesting novel avenues for targeted therapeutic strategies in glioma management.

P=N/A, N=20, Recruiting, Mayo Clinic | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026

Our study identified specific proteins as potential NMIBC biomarkers and drug targets. The identified proteins, particularly those linked to tumor recurrence and staging, warrant further validation to assess their clinical utility in NMIBC diagnosis, prognosis, and treatment strategies.

Notably, genetic deletion or pharmacological inhibition of CTSD using pepstatin A prevents immune escape and enhances anti-PD-1 efficacy. These findings identify CTSD as a key mediator of immune evasion in MSS CRC and support the development of a combination therapy comprising CTSD inhibition and anti-PD-1 immunotherapy.

In total, 94.1% of all diagnostic calls were made with 100% certainty, indicating high precision of the assay's algorithm. All analytes demonstrated acceptable analytical precision, linearity, accuracy, and stability, showing high overall analytical performance of each analyte.

These findings suggest that piperine modulates EV-mediated communication to promote apoptosis in acute leukemia. Interestingly, this work highlights the potential of piperine as a natural therapeutic agent targeting EV-mediated leukemic apoptosis.

The aberrant expression of these signature genes contributes to tumor malignant progression. Our findings offer valuable insights for future clinical research involving macrophages in TNBC.

Collectively, these findings demonstrate that SSEO exerts cytotoxic effects primarily through the induction of apoptosis in both breast and lung cancer cells, highlighting its potential as a complementary anticancer agent. The online version contains supplementary material available at 10.1007/s13205-025-04656-0.

The tracer remained stable in blood for over 2 h without causing toxicity. These findings highlight CTSD as a key cancer biomarker and demonstrate the potential of this radiotracer for improving early cancer detection and monitoring therapy response in patients.