GJB2 (Gap Junction Protein Beta 2)

P=N/A, N=18, Recruiting, Eye & ENT Hospital of Fudan University; Eye & ENT Hospital of Fudan University

TARDBP promotes HCC immune evasion and tumor growth by influencing GJB2 mRNA expression. This study identifies the TARDBP/GJB2 axis as a potential therapeutic target, offering novel strategies for HCC management.

This study demonstrates that GJB2 is a potential therapeutic target for overcoming cisplatin resistance in OC by upregulating TNC expression. Epicatechin may enhance cisplatin efficacy by targeting GJB2.

In conclusion, we established a novel prognostic model incorporating 5 CRGs that effectively predicts clinical outcomes and characterizes the immune microenvironment in OC. Our findings particularly highlight GJB2 as a key regulator of cuproptosis with significant potential as both a prognostic biomarker and therapeutic target for OC management.

P=N/A, N=0, Withdrawn, Regeneron Pharmaceuticals | N=20 --> 0 | Not yet recruiting --> Withdrawn

Parallelly, GJB2 silencing in mouse 3LL cells suppressed tumorigenesis, glycolysis, and T cell exhaustion in mice promoted by HDLBP. This research suggests that HDLBP-mediated GJB2 RNA stabilization augments glycolysis and CD8+ T cell exhaustion in LUAD progression.

P=N/A, N=20, Not yet recruiting, Regeneron Pharmaceuticals | Trial completion date: Dec 2030 --> Jun 2030 | Trial primary completion date: Nov 2026 --> Jun 2030

In conclusion, GJB2 promotes HCC progression by activating glycolysis through cytoplasmic translocation and generating a suppressive tumor microenvironment. Salvianolic acid B inhibits the expression of GJB2 and enhances the sensitivity of anti-PD1 therapy, which may provide insights into the development of novel combination therapeutic strategies for HCC.

P=N/A, N=100, Recruiting, Sensorion | Not yet recruiting --> Recruiting

P=N/A, N=100, Not yet recruiting, Sensorion

P=N/A, N=20, Recruiting, Decibel Therapeutics | Not yet recruiting --> Recruiting

Germline mutation in RUNX1 should be considered in pediatric patients with thrombocytopenia and/or abnormal platelet function and a hypocellular marrow with or without dysmegakaryopoiesis. Dysmegakaryopoiesis in the setting of RUNX1-FPDMM should not be overinterpreted as pediatric MDS without other supporting criteria such as MDS-defining cytogenetic/molecular abnormalities, multilineage dysplasia, or increased blasts. Patients with large deletions in RUNX1 may be missed on routine NGS testing hence proper germline testing in an experienced laboratory is recommended if suspicion is high.