Cholangiocarcinoma

P1, N=272, Recruiting, Pheast Therapeutics | N=155 --> 272

P=N/A, N=785, Shandong Provincial Qianfoshan Hospital; Shandong Provincial Qianfoshan Hospital

P=N/A, N=200, Shanghai Tenth People's Hospital Ethics Committee; Shanghai Tenth People's Hospital Ethics Committee

P=N/A, N=0, Completed, Hubei Cancer Hospital; Chongqing Bohao Diagnostic Technology Co., Ltd

Sensitivity analyses confirmed the robustness of these findings.ConclusionSerum NBR1, RAD51, and PARP11 are potentially causal in liver cancer pathogenesis. Specifically, the genetic regulation of PARP1 highlights a critical DNA repair mechanism, supporting their utility as predictive biomarkers.

The animal recovered uneventfully and remained clinically well with no evidence of recurrence 10 months postoperatively. This case highlights the importance of diagnostic imaging and histopathology in the evaluation of hepatic masses in reptiles and demonstrates that early surgical intervention can result in a favourable long-term outcome.

Biliary VEGF is a strong independent biomarker for the diagnosis of malignant biliary obstruction, both in PDAC and CCA. MMP-2 was independently associated with CCA diagnosis. PDGF-AA is a promising prognostic biomarker for malignant biliary strictures. These findings support the clinical potential of bile-based biomarkers for improving the diagnosis and assessing the prognosis of malignant biliary strictures.

We advocate replacing murine malondialdehyde (MDA)/glutathione (GSH) ratios with human-anchored metrics (ferritin heavy chain 1 (FTH1)/solute carrier family 40 member 1 (SLC40A1) expression, serum ferritin) and propose a "Cross-Death AI Platform" integrating network pharmacology (OmniPath/STRING), GraphSAGE deep learning (AlphaFold2 structures), and organoid validation to stratify patients and predict optimal drug combinations. By resolving spatiotemporal heterogeneity and implementing AI-guided precision medicine, we can transform multi-target interventions from empirical strategies into rational, patient-specific regimens, bridging the gap between preclinical promise and clinical success in cancers and neurodegenerative diseases.

These tumors appeared in the mutants at one week of age and caused death due to hepatic failure by 100 days. Thus, SAMD4A/B may be a promising target for anticancer drugs designed to inhibit TEAD activation.

This study uncovers a novel neuro-immune-tumour axis in iCCA and provides a mechanistic rationale for targeting β-adrenergic signalling as a possible therapeutic strategy for PNI+ iCCA.