Neuroblastoma

Mitogen-Activated Protein Kinases (MAPKs), cytosol, kinase binding, and regulation of apoptotic processes represent the key signaling pathways, cellular components, molecular functions, and biological processes involved. The results of the current study demonstrate that GSK3β and CypA contribute to clarifying the mechanisms underlying AD pathophysiology in cellular studies related to this disorder.

We have shown that 2p24.3 microduplications that include MYCN predispose to childhood embryonal tumours and should be routinely assessed when WT or neuroblastoma predisposition is suspected. We have also shown that there does not appear to be any increased incidence of childhood tumours when DDX1 alone is duplicated.

Recent advances in immunotherapy have reshaped the treatment landscape, with anti-GD2 monoclonal antibodies such as dinutuximab and naxitamab demonstrating significant clinical benefit, especially when combined with granulocyte-macrophage colony-stimulating factor (GM-CSF)...This review synthesizes current evidence on immunotherapeutic strategies in neuroblastoma, highlighting resistance pathways, biomarker-driven approaches, and the evolving clinical trial landscape. Future directions emphasize personalized, biomarker-guided immunotherapy to improve efficacy, reduce toxicity, and establish durable, curative outcomes for children with neuroblastoma.

Activation of the HIF-1α/BNIP3 pathway drives protective mitophagy to suppress the NLRP3 inflammasome in neuronal cells, thereby conferring neuroprotection against CIRI. This study provides mechanistic insights into the protective role of HIF-1α/BNIP3-mediated mitophagy against CIRI, highlighting its potential as a therapeutic target for ischemic injury.

Mechanistically, RD3 governs a self-reinforcing axis of cellular identity and immunoediting (by regulating T-cell cytokine release, activation, and cytotoxic function), positioning it as a critical checkpoint in NB evolution. These findings establish RD3 as a dual-function molecular switch and nominate RD3-targeted strategies to re-sensitize high-risk NB to immunotherapy.

P=N/A, N=214, Not yet recruiting, Beijing Children's Hospital; Beijing Children's Hospital

P=N/A, N=96, Not yet recruiting, Department of pediatric hematology and oncology, the first affiliated hospital of University of Science and Technology of China, Anhui provincial Canc

P=N/A, N=10, Recruiting, West China Hospital of Sichuan University; West China Hospital of Sichuan University | Not yet recruiting --> Recruiting

Collectively, this study elucidates the molecular mechanism by which co-exposure to PFOA, PFBA, and NPs induces neurotoxicity via suppression of mitophagy. These findings identify a potential molecular target for the prevention and treatment of PFAS- and NPs-induced neurological injury and provide valuable theoretical and experimental evidence for evaluating the neurotoxic risks of mixed environmental pollutants.

This study suggests the altered expression of ribosome biogenesis-related genes in pediatric pre-B acute lymphoblastic leukemia and neuroblastoma. The reported dysregulation suggests a disease-associated disruption in nucleolar function and translational regulation and may contribute to oncogenesis through altered ribosomal assembly, protein synthesis, or proliferative signaling.

However, when pooling all target mutations (KRAS, NRAS and BRAF), the overall sensitivity and specificity were lower, at 48.3% and 51.1%, respectively. The results of this study indicate that the ddPCR analysis of ctDNA may provide complementary information for the molecular diagnosis of CRC patients.

To the best of our knowledge, this is the first reported case of neonatal neuroblastoma with concurrent MYCN amplification and 1p deletion achieving favorable outcome through comprehensive multimodal therapy. This case underscores the importance of early diagnosis, genetic profiling, and aggressive treatment in managing high-risk neuroblastoma in neonates.