Hepatocellular Cancer

P=N/A, N=7, Terminated, National Institutes of Health Clinical Center (CC) | Phase classification: P1 --> P=N/A | Completed --> Terminated; Recruitment difficulty

P3, N=312, Not yet recruiting, Sun Yat-sen University

In hepatocellular carcinoma, mutation effect scores distinguish two tumor subclasses with different levels of β-catenin signaling, and weaker mutations predict greater immune cell infiltration in the tumor microenvironment. Our work provides a resource to understand mutational diversity within a pan-cancer mutation hotspot, with potential implications for targeted therapy.

In HepG2 cells, PFHxS modestly increased viability/DNA-synthesis readouts and enhanced NRF2 nuclear localization, NQO1 protein abundance, and MIF secretion; pharmacologic NRF2 inhibition partially attenuated NRF2/NQO1 readouts and reduced MIF secretion. Together, the data support the hypothesis that PFHxS may engage a KEAP1-NRF2-related vulnerability axis, accompanied by NRF2/NQO1 pathway readouts and increased MIF secretion, motivating exposure-characterized and genetic studies to establish causality.

This study identified NET-related key biomarkers (ECM1, DNASE1L3, JUN) as reliable diagnostic tools for HCC, highlighting their diagnostic and therapeutic potential, and providing insights for HCC diagnostic tools and immunotherapy strategies.

Trim26 attenuates liver fibrosis by stabilizing EZH2 and regulating macrophage polarization, which reduces HSC activation.

This study underscores the significant expression differences and prognostic implications of SEC13 in various cancers, emphasizing its potential as a biomarker and therapeutic target.

In individuals with HCV genotype 4, the interplay of miRNA152, DNMT1, GSTP1, and CDH1 may contribute to the pathogenesis of HCC. These indicators demonstrate potential roles as therapeutic targets and noninvasive prognostic biomarkers for HCV-related liver disease.

This hybridized apoptotic/ferroptotic pathway acts synergistically to amplify oxidative cellular damage, ultimately achieving significant suppression and eradication of hepatocellular carcinoma. This work not only provides a novel strategy for designing efficient sonosensitizers through defect engineering but also unveils a new mechanism whereby engineered sonocatalysts can treat cancer by triggering hybridized cell death pathways, offering a promising approach and theoretical foundation for the sonodynamic therapy of liver cancer.

P1/2, N=30, Recruiting, Binhui Biopharmaceutical Co., Ltd.

P2, N=35, Recruiting, Samsung Medical Center