Neuroblastoma

Our results suggest that germline loss-of-function of CREBBP may contribute to tumor predisposition factor since somatic variants of CREBBP and EP300 have been identified in neuroblastoma. Paired tumor-normal genome sequencing enabled comprehensive analysis of germline tumor predisposition, as well as genomic profiles of tumor tissue.

Conversely, TYR and OLE exhibited variable and concentration-dependent effects, also showing protection to a lesser extent, while EVOO extract proved to be more effective due to synergistic interactions among its phenolic components. Overall, CPA induces mitochondrial oxidative damage as a key mechanism of neurotoxicity, while EVOO phenolics mitigate this toxicity.

Furthermore, we review the published literature on HSCT in RALD, which includes three other patients, primarily transplanted for malignant transformation of RALD. In addition, we report our experience with targeted therapy, specifically the MEK inhibitor, in this disease and reflect on its role within the treatment paradigm of RALD.

Silencing of MELTF-AS1 augmented Zika-induced cell death, while knockdown of TIPARP-AS1, NR2F1-AS1, and SLC9A3-AS1 attenuated oncolysis, identifying lncRNAs whose modulation is associated with altered Zika-mediated cytotoxicity. These findings elucidate candidate mechanisms of Zika oncolysis in GBM cell lines, highlight novel lncRNA targets, and support further exploration of lncRNA modulation as a strategy to enhance oncolytic virotherapy for GBM and related malignancies.

Taken together, these findings suggest that A. millefolium-mediated MnO NPs exhibit notable antioxidant properties along with ROS-mediated anticancer activity. This indicates their potential as a promising and environmentally friendly nanotherapeutic approach for the treatment of neuroblastoma, although further investigation is needed to confirm their efficacy and safety.

Overall, these findings identify a phenotypic response characterized by alterations in adhesion-dependent cellular processes in neuroblastoma cells, accompanied by reduced viability and clonogenic capacity. This study provides an initial functional characterization of the biological activity of O. brasiliensis salivary gland extract in a neuroblastoma model and establishes a framework for future studies aimed at identifying the bioactive molecules responsible for these effects.

Collectively, this study demonstrates that HACE1 suppresses NB cell migration, invasion, and chemoresistance by destabilizing PKN1, thereby preventing PKN1 from phosphorylating and activating PA2G4. Our findings elucidate a novel HACE1/PKN1/PA2G4 signaling axis in NB progression, expanding the understanding of NB pathogenesis and highlighting the axis's potential as a therapeutic target.

Treatment with the CDK2/9 inhibitor fadraciclib led to significant response and an overall survival benefit in temozolomide-resistant Th-MYCN tumors and allografts generated from these resistant tumours. These findings demonstrate the utility of genetically-engineered mouse models as platforms to dissect the evolution of chemoresistance in neuroblastoma and they provide a mechanistic rationale to support the evaluation of fadraciclib in ongoing paediatric phase I studies of chemotherapy combined with temozolomide in relapsed, treatment refractory neuroblastoma patients.

In vivo, intratumoral administration of Ad-pPHOX2B-5F suppressed tumor growth in PHOX2B-positive xenografts and was associated with a reduction in PHOX2B-positive tumor areas. Together, these findings support the therapeutic potential of PHOX2B promoter-driven oncolytic adenoviruses for high-risk NB.

These findings support the utility of this RA-differentiated SH-SY5Y for neuronal-like cells for cholinergic-like model (1% HI-FBS, 10µM RA) as a practical and cost-effective platform for high-throughput AD drug screening.

In radio-resistant NB, RPT improves CAR T cells by remodeling the myeloid compartment in the TME and increasing the formation of immunological niches of cytotoxic CD8+ GZMB+ and CD4+ GZMB+ CAR T cells. While neither treatment modality alone can effectively treat NB, the combination of VLA-4-targeted RPT and GD2 or B7-H3 CAR T cells augments anti-tumor efficacy, resulting in marked tumor regression in preclinical NB models.

Therefore, ES represents a non-genotoxic mechanism to halt tumor cell growth, distinguishing it from standard cytotoxic therapies. These findings suggest that ES offers a means to suppress proliferation and induce differentiation in neuroblastoma cells, providing a potential foundation for less harmful therapeutic strategies targeting this pediatric cancer.