bims-malgli Biomed News
on Biology of malignant gliomas
Issue of 2026–09–06
six papers selected by
Oltea Sampetrean, Keio University



  1. Neuro Oncol. 2026 Aug 31. pii: noag204. [Epub ahead of print]
       BACKGROUND: Glioblastoma (GBM) is a highly aggressive brain tumor for which cell-free DNA (cfDNA) has shown promise as a minimally invasive biomarker, yet the biological processes governing cfDNA release and composition in GBM remain incompletely understood.
    METHODS: We investigated cfDNA release dynamics, fragmentation patterns, variant allele frequencies (VAF), and copy number profiles under controlled experimental conditions using patient-derived GBM cultures.
    RESULTS: Longitudinal sampling of conditioned media from monocultures revealed progressive increases in cfDNA yield that correlated more strongly with viable cell numbers than with cell death, suggesting that cfDNA production in these models is not solely driven by apoptosis. In co-culture experiments combining GBM cells with normal human astrocytes (NHA), distinct tumor- and astrocyte-specific variants enabled deconvolution of mixed-cell populations, and cfDNA composition shifted over time, consistent with increasing astrocyte death under competitive co-culture conditions. Temozolomide (TMZ) treatment altered cfDNA release dynamics, shifting the dominant source from viable cells to cell-death-associated pathways, accompanied by increased cfDNA yield, nucleosomal fragmentation, and evidence of reduced variant diversity under therapeutic pressure. Tumor-derived cfDNA was also detected and deconvolved from plasma in GBM orthotopic xenograft models, with copy number profiles recapitulating those of the parental tumor cells.
    CONCLUSION: These findings suggest that cfDNA composition is shaped by tumor proliferation, microenvironmental context, and therapeutic stress, establishing a preclinical foundation for interpreting cfDNA-based liquid biopsy signals in GBM.
    Keywords:  cell-free DNA; glioblastoma; liquid biopsy
    DOI:  https://doi.org/10.1093/neuonc/noag204
  2. Neuro Oncol. 2026 Sep 03. pii: noag213. [Epub ahead of print]
       BACKGROUND: In glioblastoma (GBM), epidermal growth factor receptor (EGFR) amplification, one of the most prevalent genetic alterations, often occurs on extrachromosomal DNAs (ecDNAs) that contain amplified oncogenes and regulatory elements, driving tumor progression. Despite the central oncogenic role of EGFR amplification, therapeutic strategies targeting EGFR have demonstrated limited clinical efficacy, suggesting that additional mechanisms may underlie EGFR-driven GBM malignancy and treatment resistance. Long non-coding RNAs (lncRNAs) are critical regulators in cancer; however, the roles of EGFR-associated lncRNAs-particularly those localized on ecDNA-in GBM tumorigenicity and therapeutic resistance remain poorly understood.
    METHODS: Transcriptomic and genomic analyses were performed to identify lncRNAs co-amplified with EGFR. Biochemical and molecular biological studies were carried out to reveal the mechanisms. In vivo xenograft models were used to evaluate the tumorigenicity and the therapeutic efficacy of combination treatment strategies.
    RESULTS: The lncRNA EGFR long non-coding downstream RNA (ELDR) was co-amplified with EGFR on ecDNA and chromosomes and was associated with poor prognosis in glioma. ELDR promoted GBM tumorigenicity through a BMI1-dependent epigenetic mechanism operating in parallel with canonical EGFR signaling. Mechanistically, ELDR interacted with purine-rich element-binding protein A (PURA), disrupted the inhibitory PURA-BMI1 interaction, and thereby enhanced the activity of BMI1, a core component of Polycomb repressive complex 1 (PRC1). Therapeutically, combining a BMI1 inhibitor or ELDR-targeting antisense oligonucleotides (ASOs) with an EGFR inhibitor erlotinib significantly enhanced antitumor efficacy in preclinical models of  EGFR  -amplified GBM with high ELDR expression.
    CONCLUSION: EGFR co-amplified ELDR promotes GBM tumorigenicity by enhancing BMI1 activity. Targeting the ELDR-BMI1 axis in combination with EGFR inhibition represents a promising therapeutic strategy for a subset of  EGFR  -amplified GBMs with high ELDR expression.
    Keywords:  EGFR; ELDR; Extrachromosomal DNA; Glioblastoma; Long non-coding RNA
    DOI:  https://doi.org/10.1093/neuonc/noag213
  3. Nat Commun. 2026 07 30. pii: 9254. [Epub ahead of print]17(1):
      Intranasal delivery offers a direct route to the brain, circumventing the blood-brain barrier (BBB) and minimizing systemic toxicity. However, its efficiency is mainly limited by the nasal mucosal barrier (NMB). Here, low-intensity pulsed ultrasound (LIPUS) without depending on the microbubbles (MBs) to amplify energy, is directly used to reversibly open the NMB by disrupting tight junction proteins. A bionic nanovesicle (iRGD-anti-programmed cell death ligand 1 (aPD-L1) & carvedilol (β-blocker) @ macrophage-derived extracellular vesicles, iMPC) is designed to co-deliver carvedilol for β-receptor blockade to reduce T-cell exhaustion, and aPD-L1 to enhance T-cell anti-tumor activity in orthotopic glioblastoma (GBM) mice during the two-hour window for NMB opening. Consequently, compared to free aPD-L1, up to a 33.38-fold increase of aPD-L1 in the GBM region is obtained with LIPUS-mediated intranasal delivery of iMPC. Reactivating T cells significantly enhances immunotherapy, leading to a 40% tumor reduction, extended survival, and long-term immune memory in orthotopic GBM mice. Overall, the LIPUS-mediated NMB opening strategy notably enhances nose-to-brain drug delivery efficiency, offering a promising platform for treating brain diseases.
    DOI:  https://doi.org/10.1038/s41467-026-76103-4
  4. Neuro Oncol. 2026 Aug 31. pii: noag199. [Epub ahead of print]
    RANO resect group
      
    Keywords:  CDKN2A/B; IDH-mutant grade 4 glioma; extent of resection; patient stratification; postoperative risk modeling
    DOI:  https://doi.org/10.1093/neuonc/noag199