ArticleActa neuropathologica communications2024
A patient-derived cell model for malignant transformation in IDH-mutant glioma.
Article in Acta neuropathologica communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Machine Learning-Based Classification of Gliomas and Tumor Grades with SHAP-Guided Feature Interpretation.Genes · 2026Article
- From Epigenetic Constraint to Evolutionary Escape: Cell-State Transitions and Selective Pressures During Malignant Transformation in Lower-Grade Gliomas.Biomedicines · 2026Review
- Malignant transformation in IDH-mutant gliomas: clinical drivers and survival outcomes in a histologically defined cohort.Journal of neuro-oncology · 2026Article
- Quantum Life Science: A Paradigm for Life Science Research.ACS nano · 2026Review
- Circulating tumor cells as a recurrence risk marker in glioma: a retrospective study.Translational cancer research · 2025Article
- Precision Oncology for High-Grade Gliomas: A Tumor Organoid Model for Adjuvant Treatment Selection.Bioengineering (Basel, Switzerland) · 2025Article
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22 authors.
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Abstract
Malignant transformation (MT) is commonly seen in IDH-mutant gliomas. There has been a growing research interest in revealing its underlying mechanisms and intervening prior to MT at the early stages of the transforming process. Here we established a unique pair of matched 3D cell models: 403L, derived from a low-grade glioma (LGG), and 403H, derived from a high-grade glioma (HGG), by utilizing IDH-mutant astrocytoma samples from the same patient when the tumor was diagnosed as WHO grade 2 (tumor mutational burden (TMB) of 3.96/Mb) and later as grade 4 (TMB of 70.07/Mb), respectively. Both cell models were authenticated to a patient's sample retaining endogenous expression of IDH1 R132H. DNA methylation profiles of the parental tumors referred to LGG and HGG IDH-mutant glioma clusters. The immunopositivity of SOX2, NESTIN, GFAP, OLIG2, and beta 3-Tubulin suggested the multilineage potential of both models. 403H was more prompt to cell invasion and developed infiltrative HGG in vivo. The differentially expressed genes (DEGs) from the RNA sequencing analysis revealed the tumor invasion and aggressiveness related genes exclusively upregulated in the 403H model. Pathway analysis showcased an enrichment of genes associated with epithelial-mesenchymal transition (EMT) and Notch signaling pathways in 403H and 403L, respectively. Mass spectrometry-based targeted metabolomics and hyperpolarized (HP) 1-
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