CTRC (Chymotrypsin C)

Integrating germline testing into surveillance redefines the management of familial PC. It uncovers hereditary susceptibility beyond classical criteria and supports cascade testing. PC also arises in mutation-negative HRI. #NCT05724992.

We identified seven potential pain modifiers in CF, including chymotrypsin C (CTRC), serine protease inhibitor Kazal-Type 1 (SPINK1), tumour necrosis factor (TNF), ATP-binding cassette subfamily B Member 1 (ABCB1), protease serine 1 (PRSS1) and transforming growth factor beta 1 (TGFB1) interacting with the CFTR gene...This in silico analysis highlights potential genes and biochemical pathways implicated in pain pathways that could significantly impact pain perception in people living with CF and their response to prescribed therapies. Further functional analyses are needed to include CF participants and provide a physiological relevance on how genetic polymorphisms of identified GMs may impact their pain phenotype or profile.

This study establishes a visceral pain model centered on pancreatic parenchymal nociception rather than secondary neural effects, and for the first time proposes an interconnected regulatory network linking epigenetic modifications, immune reprogramming, and neural plasticity, revealing dual pain pathogenesis mechanisms: (1) immune microenvironment reshaping that potentiates neuroinflammation, and (2) direct ion channel regulation enhancing neuronal excitability. These findings provide a mechanistic foundation for developing methylation-based prognostic biomarkers and multimodal analgesic therapeutic strategies targeting the immuno-neural nexus.

This study identifies CTRC/PRDX1/SKP1 as crucial and proposes hypothesis of synergistic effects between exposure and infection history. These findings underscore incorporating environmental exposure into risk assessment, offering perspectives on carcinogenesis and avenues for prevention.

P3, N=9000, Recruiting, Johns Hopkins University | Trial completion date: Dec 2025 --> Jun 2029 | Trial primary completion date: Oct 2025 --> Dec 2028

P1, N=66, Recruiting, University of Colorado, Denver | Trial primary completion date: Dec 2025 --> May 2026

Despite its small scale, the findings highlight the utility of scRNA-seq in veterinary oncology and its translational potential for pancreatic neuroendocrine tumours across species. The online version contains supplementary material available at 10.1186/s44356-025-00026-3.

P=N/A, N=150, Recruiting, University of Colorado, Boulder | Trial completion date: Jan 2027 --> Feb 2028 | Trial primary completion date: Jul 2026 --> Nov 2027

P1, N=66, Recruiting, University of Colorado, Denver | Trial completion date: Oct 2025 --> Nov 2026 | Trial primary completion date: Dec 2024 --> Dec 2025

ACEi/ARBs therapy was not associated with a reduction in CTRC among patients with cancer receiving anthracyclines. However, there were favorable changes in LVEF and left ventricular remodeling with ACEi/ARBs therapy. Further large-scale studies are needed to better understand the potential role of ACEi/ARBs in preventing long-term cardiotoxicity.

In vivo experiments also indicated that silencing miR-486-3p inhibited PDAC malignant progression and immunosuppressive factor expression in vivo. In summary, miR-486-3p promotes immunosuppressive factor protein expression by targeting and negatively regulating CTRC expression, which in turn promotes PDAC malignant progression.

Plasma alpha-1-antichymotrypsin correlated with the estimated burden of pulmonary KS in the respiratory tract (r = 0.439; p = .0002) and 234 μg/ml had 51% sensitivity and 94% specificity for detection of pulmonary KS by bronchoscopy. Measurement of plasma alpha-1-antichymotrypsin has potential for identifying persons with pulmonary AIDS-KS and estimating the burden of KS in the lower respiratory tract.