Brain Cancer

P1, N=61, Active, not recruiting, Institute of Cancer Research, United Kingdom | Recruiting --> Active, not recruiting | Trial completion date: Mar 2026 --> Dec 2026 | Trial primary completion date: Mar 2026 --> Dec 2026

P2, N=31, Recruiting, Second Affiliated Hospital, School of Medicine, Zhejiang University

In each scenario, the donor cells' exosomal cargo modulates recipient cell functions, promoting tissue repair, immune regulation, or metastasis. This work expands the conceptual framework of exofection and emphasizes its potential impact on therapeutic development and understanding the pathophysiology of various diseases.

PAXBP1-AS1, as a diagnostic biomarker in VS-related HL, can affect HEI-193 cell viability, apoptosis, and inflammatory level by targeting and negatively regulating the miR-124-3p.

In conclusion, this study demonstrates that rs1136410 is significantly associated with brain tumor risk particularly with the glioma and meningioma subtypes underscoring the role of PARP1 in brain tumor genetics and its potential as a therapeutic target.

Our results indicate that oral STF treatment is associated with improvements in social behavior, myelination, and gut microbial composition in offspring with perinatal injury, underscoring the need for future studies to elucidate the potential causal relationships among these outcomes.

The top-ranked miRNAs were also analysed and compared with biomarkers previously known from the literature. Seven miRNAs were identified as potential biomarkers, namely the miR-125a-3p, miR-4276, miR-4648, miR-4763-3p, miR-663a, miR-6784-5p and miR-873-3p, and were independently validated on the GSE211692 dataset.

The authors conclude that ecDNA amplification serves as a credible adverse prognostic indicator and holds promise for refining risk stratification and guiding treatment strategies. However, they stress that clinical adoption remains constrained by the absence of standardized, scalable, and reproducible detection.

These findings suggest that lactylation may modulate DNA repair and therapeutic response in a context-dependent manner. Targeting lactate metabolism, transport and lactylation regulators, including LDHA, MCT1/4, ACAT1, AARS1 and GCN5, or using site-specific lactylation-inhibiting peptides may improve chemotherapy and PARP inhibitor efficacy, but clinical translation remains limited by heterogeneity, metabolic plasticity, toxicity and insufficient validation.

Mechanistically, ChIP-qPCR demonstrated that RA treatment or ALDH1A3 overexpression increased RARα occupancy at the PAI-1 regulatory region, accompanied by increased PAI-1 expression, both of which were diminished by AGN. Collectively, the present study defines an ALDH1A3-RA-PAI-1 signaling axis that contributes to GBM cell motility and invasion.

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.

Finally, we distinguish disulfidptosis, whose direct relevance to CAR-T-cell responses remains to be established, from glycosylation and glycocalyx remodeling as more direct determinants of target-antigen accessibility and immune recognition. Therapeutic strategies addressing these vulnerabilities may provide rational opportunities to improve CAR-T-based and combinatorial therapies for GB.