Neuroblastoma

The RUVBL proteins form a complex with ATPase activity that has broad cellular functions and we demonstrate that pharmacological inhibition of this protein complex results in a strong reduction of MYC(N) signaling, cell-cycle arrest, DNA damage, and apoptosis. We confirmed the association with MYCN and identified the RUVBL genes as independent prognostic biomarkers in human primary neuroblastoma data.

Understanding its complex biology is critical for the development of novel immunotherapies aimed at restoring effective anti-tumor immune responses, particularly in high-risk MYCN-amplified NB. Targeting the CCL2 axis represents a promising strategy to improve NB patient outcomes.

Collectively, these findings demonstrate that capsaicin confers protection against MGO-induced neuronal toxicity through coordinated activation of the TRPV1-PERK-ATF4-Sestrin2 stress-response pathway and direct chemical neutralization of MGO. Our results identify capsaicin as a dual-function modulator of carbonyl stress and suggest its potential relevance for therapeutic strategies targeting MGO-associated neurotoxicity.

Mechanistically, Mn@CDs downregulate NOX2/NOX4 within RVLM region and alleviate oxidative stress, thus reversing microglial activation and reducing neuronal apoptosis. This work presents a non-pharmaceutical catalytic strategy based on biocompatible Mn@CDs nanozymes targeting the RVLM ROS-neuroinflammation axis for SIH.

MALDI mass spectrometry imaging confirmed oxidized CoQ10 accumulation in myocardial tissue beyond the vasculature, consistent with UHPLC-MS/MS findings. These results demonstrate that BPM31510 targets bioactive CoQ10 to metabolically active tissues, overcoming limitations of oral supplementation, and may provide therapeutic benefit for primary and secondary CoQ10 deficiencies and other mitochondrial or metabolic disorders marked by impaired redox balance and energy homeostasis.

P3, N=43, Active, not recruiting, Innervate Radiopharmaceuticals LLC (Formerly: Illumina Radiopharmaceuticals LLC) | Completed --> Active, not recruiting | Trial completion date: May 2024 --> Aug 2026 | Trial primary completion date: May 2024 --> Jul 2026

Together, these findings reveal a phosphorylation-independent mechanism by which JAK2 stabilizes Nurr1 protein and enhances its transcriptional activity. Our results further suggest that age-associated induction of JAK2 in dopaminergic neurons may promote neuronal resilience by maintaining Nurr1 protein stability during aging.

Everolimus (EVER) and tozasertib (TOZA) encapsulated in NP and targeted with dinutuximab β (DTX-β). DTX-β/EVER-TOZA@PEG-b-PLGA may exert cytotoxic and apoptotic effects in NB. The use of targeted nanocarriers in NB treatment may enhance cytotoxic and apoptotic responses specifically in the tumor region.

P2, N=94, Recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Mar 2026 --> Mar 2027 | Trial primary completion date: Mar 2026 --> Mar 2027

FD metrics derived from contrast-enhanced CT images are significantly associated with established clinical/pathological risk factors and overall survival in pediatric neuroblastoma. FD may serve as a non-invasive imaging biomarker to assist in risk stratification and clinical decision-making.

ELF magnetic field exposure caused intensity dependent nuclear abnormalities, increased oxidative DNA lesions, early oxidative imbalance, and a predominance of necrotic over apoptotic cell death. These findings indicate that continuous low-intensity ELF magnetic field exposure disrupts redox homeostasis and compromises genomic stability in differentiated neuronal cells.

The virus entry process requires the functional cooperation of clathrin, dynamin, and Eps15, followed by trafficking through Rab5-positive early endosomes and Rab7/Rab9-positive late endosomes in an acidification-dependent manner. This comprehensive understanding of BATV entry mechanisms provides a theoretical foundation for developing targeted antiviral strategies and therapeutic interventions against BATV-associated neurological diseases.