Eye Cancer

ASPHD1 overexpression also upregulated neuronal differentiation-related genes, produced more negative resting membrane potentials on whole-cell patch-clamp recordings, enhanced depolarization-evoked Ca2+ transients on calcium imaging, and increased NeuN protein expression. Together, these findings identify ASPHD1 as a favorable prognostic biomarker in glioma and suggest that high ASPHD1 expression restrains glioma progression while promoting neuron-like differentiation of glioma cells.

Therefore, further investigation of how PRIM1 is regulated in this cancer type is essential. This association between PRIM1 and advanced urothelial carcinoma highlights the crosstalk between DNA replication machinery and genetic mutations in bladder cancer, which may open new possibilities for targeted therapies and biomarker discovery.

P2, N=85, Active, not recruiting, iOnctura | Recruiting --> Active, not recruiting

The integration of AH liquid biopsy in RB management may aid prognosis prediction and optimize treatment strategies. However, further research is needed to validate the prognostic significance.

In addition, we review the status of AURKA-specific inhibitors in clinical evaluation and their associated adverse effects. Finally, we cite the emerging therapeutic strategy of proteolysis targeting chimeras (PROTACs) as an innovative means to selectively degrade AURKs, offering a novel approach to targeted cancer therapy.

In vivo, NAT10 promoted tumor growth. Collectively, NAT10 contributes to RB progression by enhancing glycolysis through ac4C-mediated PFKFB3 mRNA stabilization, identifying the NAT10-ac4C-PFKFB3 axis as a potential therapeutic target.

P=N/A, N=108, Active, not recruiting, Jonsson Comprehensive Cancer Center | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2026

MBD4 downregulation significantly impaired carboplatin or etoposide efficacy in vitro and in vivo, respectively. In the present study, our findings indicate that depletion or mutation of MBD4 interferes with the activation of the cell cycle and apoptosis via epigenetic regulation, thereby reducing drug susceptibility. It provides new insights into the role in RB chemoresistance of MBD4 as an epigenetic regulator, which might fuel the development of new RB-targeted strategies.

Disruption of redox equilibrium by enhancing reactive oxygen species (ROS) via a mitochondria-targeted oxidative phosphorylation inhibitor triggered endoplasmic reticulum stress and downregulated SPP1 expression, thereby defining a direct metabolic-immune regulatory axis. Together, our findings reveal a previously unrecognized ROS-SPP1-CD44 axis that links tumor redox homeostasis to immune evasion, providing mechanistic insight into the immune-resistant phenotype of UM and suggesting potential therapeutic vulnerabilities within the metabolic-immune crosstalk.

The PIEZO1-DOT1L axis mediated ECM stiffness-driven stemness and tumor progression in UM. Targeting this mechanotransduction pathway by modulating ECM stiffness or its downstream effectors may provide a novel therapeutic strategy for UM.

LP-WGS appears feasible for SCNAs detection in FFPE uveal melanoma specimens, including cases previously treated before enucleation, and holds promise to inform prognostic stratification in this rare tumor type. The successful application of LP-WGS to FFPE uveal melanoma specimens supports prospective investigations in rare cancers and may enable the development of personalized treatment strategies.

Our findings demonstrate, for the first time, that nRPCs are the most sensitive cells to RB1 loss inducing abnormal proliferation of nascent retinal cells, while ATOH7+ nascent CPs represent the earliest cellular origin of human Rb. These insights may facilitate the development of targeted therapies for Rb.