Anaplastic Astrocytoma

These findings contribute to the literature suggesting that, rarely, GPV in aoCPG may contribute to cancer diagnoses in children, raising the question of how tumors in these cases may present differently in children than adults. Increased knowledge about potential childhood cancer risks related to what have historically been considered aoCPG could modify predictive genetic testing recommendations for children and enhance existing cancer screening protocols.

Finally, we discuss therapeutic directions spanning AQP4 modulation, isoform balance, and BBB-bypassing delivery strategies. Overall, AQP4 emerges as a mechanistic hub connecting BBB instability, glymphatic impairment, edema, immune evasion, and invasion in GBM.

This case represents the first report of a BCOR ITD in an IDH-mutant WHO grade 4 astrocytoma. The discovery expands the molecular spectrum of high-grade astrocytomas and highlights the need for further research into the biological, prognostic, and therapeutic significance of BCOR alterations in these tumors.

P1, N=18, Active, not recruiting, City of Hope Medical Center | Trial completion date: Oct 2025 --> Sep 2026

P2, N=38, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Oct 2025 --> Oct 2026

P2, N=120, Recruiting, Nationwide Children's Hospital | Trial primary completion date: Aug 2028 --> Aug 2029

CTV < 127 cm3 predicted longer OS in grade 4 gliomas (3.2 vs. 1.7 years, p = 0.012). Our findings provide new real-world evidence on survival and prognostic factors in this population, for which contemporary RWE and OS/PFS data remain scarce.

P1, N=15, Active, not recruiting, Nationwide Children's Hospital | Trial primary completion date: Jul 2028 --> Jul 2029

P1, N=20, Recruiting, Mayo Clinic | Trial completion date: Jul 2025 --> Jul 2026 | Trial primary completion date: Jul 2025 --> Jul 2026

Preclinical work demonstrates the chemopotentiating effect of LDFRT. In our clinical trial, LDFRT with temozolomide was safe and well-tolerated in patients with recurrent HGG receiving salvage re-irradiation. Although the primary survival endpoint was not achieved, high pseudoprogression rates at low radiation doses support the principle of low-dose radiation hypersensitivity mediated by chemopotentiation and potentially immune-modulation.

Our results reveal that inhibition of TRAF3IP2 in glioblastoma cells attenuates metabolic activity, as evidenced by decreased expression levels of NAMPT and the mTOR complex, leading to reduction in NAD synthesis and glycolytic function, decreased expression of NAD-dependent deacetylase SIRT1, and increased presence of cellular ROS and expression of tumor suppressor p53, cumulatively resulting in decreased cell viability in glioblastoma. These outcomes elucidate that inhibition of TRAF3IP2 exerts significant anti-tumor effects on glioblastoma by reducing NAD availability and cancer-cell metabolism, highlighting the therapeutic potential of TRAF3IP2 in glioblastoma.

On the other hand, Octreotide notably reduced CD31 expression, inhibiting angiogenesis and effectively suppressing both tumor growth and glioma cell proliferation in the in vivo study. It holds potential as a valuable approach for post-resection management of GBM, preceding standard chemo-radiation therapy.