OLIG2 (Oligodendrocyte Transcription Factor 2)

The humane endpoint was reached after 6-8 weeks, allowing for timely treatment intervention and monitoring of tumor progression. Therefore, the AMG5 line provides a new tool in glioma research by generating reproducible GBM with features of mesenchymal subtype to address emerging questions and to better understand GBM development.

Inhibition of PA synthesis restored Olig2 expression, improved myelination, and rescued differentiation deficits in PWMI mice. Collectively, this study identifies PA as a potential metabolic risk factor associated with preterm CP and uncovers a PA-TRIM59-Olig2 signaling axis linking lipid metabolism to OPC differentiation failure and PWMI.

These findings suggest that stigmasterol confers neuroprotection by preserving oligodendrocyte lineage cells, enhancing PDGFRα-mediated precursor recruitment, and maintaining myelin integrity. By mitigating neuroinflammation and promoting remyelination, stigmasterol is a promising therapeutic candidate for metal-induced demyelinating disorders.

Doses needed to eliminate OLIG2 expression in vitro varied from 0.3 to >1 µM in pGBM cells. In summary, our data showed that orally administered CT-179 penetrated the blood-brain barrier (BBB) and exhibited potential for inhibiting pGBM growth when combined with XRT.

Molecular simulations indicated stable puerarin-cGAS interactions, validated experimentally: puerarin suppressed cGAS-STING activation, reduced oligodendrocyte apoptosis, and promoted remyelination. These results provide new insights into ICH pathogenesis and support puerarin as a potential therapeutic agent for BBB disruption and WMI.

Interestingly, a persistent ASCL1 expression also maintains OPCs into postnatal stages by promoting their self-renewal while suppressing their differentiation into postmitotic oligodendrocytes. Together, these findings establish ASCL1 as a key regulator of the spatiotemporal order of glial lineage diversity in cortical GM and callosal WM and implicate ASCL1 dysregulation as an underlying mechanism in the pathogenesis of gliomas.

Cases 1 and 2 were strongly immunoreactive to CNPase and had robust immunoreactivity to GFAP. This case series highlights that Wright-Giemsa intra-operative squash preparations stain can support a presumptive diagnosis of oligodendroglioma.

This case underscores the need to include PGNT in the differential diagnosis of pediatric patients presenting with new-onset focal seizures and MRI findings suggestive of a low-grade glioma. Surgical management is typically curative, resulting in excellent seizure control and long-term outcomes.

Here, we show that the oligodendrocyte markers olig1 and plp1b are not expressed in MEP glia. These findings refine the molecular signature of MEP glia, enhancing their peripheral identity.

Collectively, a TP53 abnormality at copy number (12/26, all cnLOH), sequence (55/60) and protein expression (46/48) level was detected in all 60 cases. In conclusion, integrated high-resolution copy number and histomolecular analysis expanded the spectrum of genetic changes associated with DHG-H3 G34, including the presence of universal TP53 abnormalities with frequent cnLOH-a copy number abnormality that has been largely unrecognized-for this new 2021 World Health Organization central nervous system tumor type.

They also represent the first PLAG1 fusions identified in pediatric supratentorial ependymal tumors. These cases highlight the value of integrating histology, methylation profiling, and fusion detection, and suggest a new candidate supratentorial ependymal subtype with PLAG1 fusions, pending validation in larger series.

A second population of large round cells with abundant cytoplasm had positive cytoplasmic staining for S100 protein and synaptophysin (SYN), compatible with mature neurons. We diagnosed a spinal cord ganglioglioma in this steer based on histologic features and OLIG2 and SYN immunolabelling.