Glioma

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.

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.

AD and glioblastoma are connected by common neuroinflammatory pathways, but these processes result in neurodegeneration in AD and tumor support in glioblastoma. Understanding these shared and divergent mechanisms may guide the development of biomarkers and targeted therapies focused on microglia, inflammasomes, cytokines, and immune reprogramming in both diseases.

In human GBM, the C5a/C5aR1 axis is activated and positively correlates with stemness, immunosuppressive TAMs and predicts poor prognosis. Collectively, these results demonstrate the key role of C5a/C5aR1 pathway in GSCs-TAMs symbiosis and indicate the therapeutic potential of targeting this pathway for GBM treatment.

In vivo, CTS suppressed tumor growth and activated ferroptosis, whereas EGFR overexpression partially reversed these protective effects. CTS induces ferroptosis in glioma cells by inhibiting EGFR and enhancing ROS signaling, thereby suppressing tumor proliferation and invasion.

In contrast, miR-340 was downregulated in glioma cells, and its direct transfection markedly inhibited proliferation without astrocyte toxicity; fluorescent miR-340 was also detected within TMs and recipient glioma cells. Together, these findings identify TMs as structural features shaped by IDH1 mutation and as conduits for intercellular exchange of both oncogenic and tumor-suppressive microRNAs, providing a framework for understanding TM-mediated communication and its potential therapeutic exploitation in glioma.

This NUP54-associated phenotype was attenuated by the HIF-1α inhibitor PX-478 in vitro and in vivo. Overall, this study identifies NUP54 as a potential prognostic biomarker in LUAD and suggests that the NUP54/HIF-1α/glycolysis-related pathway may represent a biological mechanism worthy of further investigation.

Notably, BRAF/MEK inhibition disrupts interferon programs and tumor-microglia interactions in BRAFV600E ex vivo in human GBM/brain slice cultures. Our findings elucidate that tumor-intrinsic MAPK/ERK promotes immunotherapy response, interferon responses, T cell tumor infiltration, and GBM cell-microglia interactions.

CAMK2A regulates glioma cell proliferation through the Ras/Raf/MEK/ERK signaling pathway. CAMK2A is a potentially important target for glioma therapy.

P=N/A, N=22, Completed, Central Hospital, Nancy, France | Not yet recruiting --> Completed