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BIOMARKER:

IDH wild-type

i
Other names: HEL-216, HEL-S-26, Epididymis Luminal Protein 216, Isocitrate Dehydrogenase 1 (NADP+), Epididymis Secretory Protein Li 26, IDH1, Isocitrate Dehydrogenase (NADP(+)) 1, Isocitrate Dehydrogenase 1 (NADP+), Soluble, IDH2, Isocitrate Dehydrogenase (NADP(+)) 2, Isocitrate Dehydrogenase (NADP(+)) 2, Mitochondrial, Isocitrate Dehydrogenase 2 (NADP+), Mitochondrial, Isocitrate Dehydrogenase [NADP], Mitochondrial, Oxalosuccinate Decarboxylase, NADP(+)-Specific ICDH, ICD-M, IDH, IDP, MNADP-IDH, D2HGA2, IDHM, IDPM
Entrez ID:
Related biomarkers:
3d
AI-based pathomics model predicts regulatory T cell infiltration and radiotherapy response in IDH-wild-type glioblastoma. (PubMed, Front Immunol)
Gene set enrichment analysis linked high PS to immune-evasive pathways, including Notch and IL-6/JAK/STAT3 signaling, along with increased expression of DNA repair gene RAD50, suggesting a potential association with radiotherapy response. This AI-based pathomics framework offers a robust and interpretable tool for immunoprofiling and outcome prediction, paving the way for precision radiotherapy and Treg-targeted therapeutic strategies in glioblastoma.
Journal
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IL6 (Interleukin 6) • RAD50 (RAD50 Double Strand Break Repair Protein)
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IDH wild-type
3d
Optimal clinicogenetic criteria for post-operative re-irradiation in recurrent glioblastoma: KROG 21-02. (PubMed, ESMO Open)
Post-operative re-RT appears to be associated with enhanced survival and minimal toxicity in patients with rGBM following temozolomide chemoradiation. Our study suggests a novel clinicogenetic criterion for re-RT after re-OP in rGBM, which requires further validation.
Journal
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CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B)
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CDKN2A deletion • IDH wild-type
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temozolomide
4d
Enrollment open
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IDH wild-type
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lomustine
6d
Study of Acetazolamide With Temozolomide in Adults With Newly Diagnosed or Recurrent Malignant Glioma (clinicaltrials.gov)
P1, N=10, Active, not recruiting, University of Chicago | Trial primary completion date: Jun 2025 --> Dec 2026
Trial primary completion date
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IDH wild-type
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temozolomide • acetazolamide
6d
Expanding the spectrum of H3K27-altered gliomas: Hemispheric cases with midline epigenetic signatures. (PubMed, Ann Diagn Pathol)
Clinically, two patients died within 3-9 months, while one remains clinically stable despite radiological progression. DHG-H3 K27 represents a rare hemispheric glioma subgroup sharing molecular and epigenetic features of DMG-H3 K27 without midline involvement, underscoring biological heterogeneity and the importance of integrated molecular classification.
Journal
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BRAF (B-raf proto-oncogene) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR1 (Fibroblast growth factor receptor 1) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • NF1 (Neurofibromin 1) • ATRX (ATRX Chromatin Remodeler) • H3-3A (H3.3 Histone A)
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BRAF mutation • PIK3CA mutation • IDH wild-type
6d
Glioblastoma treatment patterns and outcomes over 18 years in an Irish cancer centre. (PubMed, Ir J Med Sci)
Despite advances in our understanding of the pathogenesis of glioblastoma, the mOS median overall survival in our real-world patient cohort did not improve over time. The findings emphasise the need for ongoing research efforts to improve outcomes in this lethal disease.
Journal
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MGMT (6-O-methylguanine-DNA methyltransferase)
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IDH wild-type
7d
GLOW: Glioblastoma Targeted Treatment Option Maximization by WGS (clinicaltrials.gov)
P=N/A, N=164, Completed, UMC Utrecht | Recruiting --> Completed | Trial completion date: Jul 2025 --> Dec 2025 | Trial primary completion date: Jul 2024 --> Sep 2025
Trial completion • Trial completion date • Trial primary completion date
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IDH wild-type
7d
Murine modeling of IDH-mutant 1p/19q-codeleted oligodendroglioma reveals genotype specific phenotypes. (PubMed, bioRxiv)
Oligo Cdkn2a tumors displayed metabolic and transcriptional changes associated with IDH and CIC mutations, and single cell sequencing identified a bias towards oligodendrocyte differentiation compared to an IDH wild-type glioblastoma mouse model. Oligo Cdkn2a tumors represent the first mouse model system to recapitulate the genetic, histological and transcriptional features of human IDH-mutant 1p/19q-codeleted oligodendrogliomas, offering a platform to further dissect tumor biology and test new therapeutic strategies.
Preclinical • Journal
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TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • FUBP1 (Far Upstream Element Binding Protein 1)
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TP53 mutation • IDH wild-type • IDH1 R132
7d
Report of treatment intensity and survival outcomes in older patients with glioblastoma diagnosed according to WHO CNS 5 classification. (PubMed, J Neurooncol)
This international clinical dataset of adults diagnosed with glioblastoma since the introduction of the WHO CNS 5 criteria supports the use of conventionally fractionated chemoradiation in fit patients < 70, while hypofractionated regimens are appropriate for those ≥ 70. Surgical extent, treatment intensity, and MGMT methylation remain key determinants of survival in older patients with glioblastoma.
Journal
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MGMT (6-O-methylguanine-DNA methyltransferase)
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MGMT promoter methylation • IDH wild-type
8d
Primary Mismatch Repair Deficient Glioma (PMMRDG), IDH-wildtype and H3-wildtype: A Giant Cell Tumor with Potential for Long-Term Survival Occurring at all Ages. (PubMed, Neuro Oncol)
Overall, our findings indicate that PMMRDGs represent a distinct type of IDH-wildtype gliomas with potential for long-term survival likely driven by immune activation.
Journal • Mismatch repair • Tumor mutational burden • dMMR
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TMB (Tumor Mutational Burden)
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TMB-H • MSI-H/dMMR • IDH wild-type
8d
Acquired genetic and cell-state changes in IDH-mutant glioma progression. (PubMed, Nature)
Second, increased mesenchymal-like-state abundance occurred independently of acquired genetic alterations and instead coincided with elevated macrophage expression. Overall, our findings provide an integrative model that traces the cell intrinsic and extrinsic factors that shape cellular states during IDH-mutant glioma disease progression.
Journal
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PDGFRA (Platelet Derived Growth Factor Receptor Alpha)
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IDH wild-type