ArticleBrain pathology (Zurich, Switzerland)2023
Genomic profiling and prognostic factors of H3 K27M-mutant spinal cord diffuse glioma.
Article in Brain pathology (Zurich, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pediatric-type high-grade glioma of the spinal cord in the molecular era: institutional case series and updated systematic review of the literature.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2025Pooled it
- Understanding DMG: current treatment options and prospective solutions using nanoparticles.Drug delivery and translational research · 2026Review
- Radiomics-guided multimodal MRI fusion framework for non-enhanced glioblastoma noninvasive identification.PLOS digital health · 2026Article
- Application of a multimodal MRI model integrating radiomics and habitat features for predicting glioma pathology and prognosis.BMC medical imaging · 2026Article
- Targeting WTAP/ROR1/WNT5A-Mediated Crosstalk Between Glioma Stem Cells and Macrophages to Normalize Tumor Vasculature and Enhance Chemotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A multimodal ConvNeXt-Tiny deep learning model for simultaneous prediction of IDH mutation and Ki-67 expression in gliomas.PloS one · 2026Article
- Adult spinal cord diffuse midline gliomas with piloid features have a better prognosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- H3F3B p.K27I-mutant diffuse midline glioma is a distinct subtype of H3K27-altered diffuse midline glioma.Acta neuropathologica communications · 2025Article
- GD2: hopes and challenges for the treatment of pediatric patients with tumors of the central nervous system.NPJ precision oncology · 2025Review
- Ara-C suppresses H3 K27-altered spinal cord diffuse midline glioma growth and enhances immune checkpoint blockade sensitivity.Science advances · 2025Article
- Cellular Heterogeneity and IL-17 Pathway Dynamics Reveal Insights into the Transition from Ulcerative Colitis to Colorectal Cancer Through scRNA-Seq Analysis.Journal of inflammation research · 2025Article
- Clinico-Pathological Features of Diffuse Midline Glioma, H3 K27-Altered in Adults: A Comprehensive Review of the Literature with an Additional Single-Institution Case Series.Diagnostics (Basel, Switzerland) · 2024Article
- Specifics of spinal neuropathology in the molecular age.Neuro-oncology advances · 2024Review
- The Role of Radiotherapy, Chemotherapy, and Targeted Therapies in Adult Intramedullary Spinal Cord Tumors.Cancers · 2024Review
- Article
- Methylation class oligosarcoma, IDH-mutant could exhibit astrocytoma-like molecular features.Acta neuropathologica · 2024Article
- Sequencing of cerebrospinal fluid cell-free DNA facilitated early differential diagnosis of intramedullary spinal cord tumors.NPJ precision oncology · 2024Article
- Current and future therapeutic strategies for high-grade gliomas leveraging the interplay between epigenetic regulators and kinase signaling networks.Journal of experimental & clinical cancer research : CR · 2024Review
- Pediatric CNS tumors and 2021 WHO classification: what do oncologists need from pathologists?Frontiers in molecular neuroscience · 2024Review
- Does H3K27M Mutation Impact Survival Outcome of High-Grade Spinal Cord Astrocytoma?Neurospine · 2023Article
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14 authors.
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Abstract
H3 K27-altered diffuse midline glioma is a highly lethal pediatric-type tumor without efficacious treatments. Recent findings have highlighted the heterogeneity among diffuse midline gliomas with different locations and ages. Compared to tumors located in the brain stem and thalamus, the molecular and clinicopathological features of H3 K27-altered spinal cord glioma are still largely elusive, thus hindering the accurate management of patients. Here we aimed to characterize the clinicopathological and molecular features of H3 K27M-mutant spinal cord glioma in 77 consecutive cases. We found that the H3 K27M-mutant spinal cord glioma, with a median age of 35 years old, had a significantly better prognosis than H3 K27M-mutant brain tumors. We noticed a molecular heterogeneity of H3 K27M-mutant spinal cord astrocytoma via targeted sequencing with 34 cases. TP53 mutation which occurred in 58.8% of cases is mutually exclusive with PPM1D (26%) and NF1 (44%) mutations. The TP53-mutant cases had a significantly higher number of copy number variants (CNV) and a marginally higher proportion of pediatric patients (age at diagnosis <18 years old, p = 0.056). Cox regression and Kaplan-Meier curve analysis showed that the higher number of CNV events (≥3), chromosome (Chr) 9p deletion, Chr 10p deletion, ATRX mutation, CDK6 amplification, and retinoblastoma protein (RB) pathway alteration are associated with worse survival. Cox regression analysis with clinicopathological features showed that glioblastoma histological type and a high Ki-67 index (>10%) are associated with a worse prognosis. Interestingly, the histological type, an independent prognostic factor in multivariate Cox regression, can also stratify molecular features of H3 K27M-mutant spinal cord glioma, including the RB pathway, KRAS/PI3K pathway, and chromosome arms CNV. In conclusion, although all H3 K27M-mutant spinal cord diffuse glioma were diagnosed as WHO Grade 4, the histological type, molecular features representing chromatin instability, and molecular alterations associated with accelerated cell proliferative activity should not be ignored in clinical management.
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