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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
Clinical • Retrospective data • Journal
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TERT (Telomerase Reverse Transcriptase)
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IDH wild-type
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temozolomide
3d
Unveiling the prognostic and immunological role of IFI44 in glioma. (PubMed, Ann Med)
IFI44 may drive glioma progression through dual mechanisms of immune microenvironment remodeling and promotion of tumor cell aggressiveness, supporting its potential as a prognostic biomarker and therapeutic target. Although preliminary knockdown and overexpression assays were performed, the underlying mechanisms of IFI44-mediated immune regulation and tumor progression require further investigation.
Journal • PD(L)-1 Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • NOTCH1 (Notch 1) • NF1 (Neurofibromin 1) • PD-1 (Programmed cell death 1) • LAG3 (Lymphocyte Activating 3)
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PD-L1 expression • IDH wild-type
4d
Predicting short-term recurrence and identifying key risk factors in elderly glioma patients: Insights from a retrospective cohort study. (PubMed, Clin Neurol Neurosurg)
Both pre- and postoperative models successfully predict short-term recurrence in elderly glioma patients. Key clinical risk factors, such as tumors infiltrating the corpus callosum and various tumor-related symptoms were identified. Additionally, certain common postoperative physical and psychological symptom changes in the MDASI-BT may be predictive markers for long-term relapse. A crucial finding is that the factors associated with recurrence are distinct across molecular subtypes, underscoring the need for subtype-specific risk management.
Retrospective data • Journal
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TP53 (Tumor protein P53) • MGMT (6-O-methylguanine-DNA methyltransferase)
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TP53 mutation • MGMT promoter methylation • IDH wild-type
6d
Optimal qMSP cutoff value for MGMT promoter methylation in glioblastoma and its validation for clinical significance. (PubMed, BMC Cancer)
The identified qMSP cut-off value (0.242) based on the procedure described in this study provides a robust prognostic stratification tool for GBM patients. High MGMT methylation correlates with improved survival, supporting its integration into clinical decision-making. Further multi-center validation studies are warranted to establish standardized MGMT assessment methodologies.
Retrospective data • Journal
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MGMT (6-O-methylguanine-DNA methyltransferase) • TERT (Telomerase Reverse Transcriptase)
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MGMT promoter methylation • IDH wild-type
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temozolomide
9d
rhIL-7-hyFc on Increasing Lymphocyte Counts in Patients With Newly Diagnosed Non-severe Lymphopenic Gliomas Following Radiation and Temozolomide (clinicaltrials.gov)
P1/2, N=42, Active, not recruiting, Washington University School of Medicine | Trial completion date: Jan 2032 --> Apr 2028
Trial completion date
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • MGMT (6-O-methylguanine-DNA methyltransferase)
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IDH wild-type • IDH1 R132
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temozolomide • Hyleukin-7 (efineptakin alfa)
9d
Single-cell multi-omics identifies metabolism-linked epigenetic reprogramming as a driver of therapy-resistant medulloblastoma. (PubMed, Nat Commun)
IDH1 inhibition reverses resistance-mediated chromatin changes and enables radiation re-sensitization. Ultimately, these findings demonstrate the efficacy of single-cell multiome analysis in elucidating resistance mechanisms and identifying targetable pathways for MYC-driven medulloblastoma.
Journal
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1)
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IDH wild-type
10d
RNaseH2 inhibition potentiates temozolomide response in patient derived glioblastoma cells. (PubMed, Sci Rep)
We selected six of these inhibitors for further investigation, evaluating their effects both alone and in combination with TMZ in commercially available U87 MG wild-type and IDH1 mutant (IDH1 WT and MUT) glioma cells and patient-derived cells established from glioma organoids (GBO-PDC). This study highlights the therapeutic potential of RNaseH2 inhibition in combination with TMZ for GBM therapy, validated in patient-derived model, offering a promising avenue for treating this highly aggressive and yet uncurable cancer.
Journal • Tumor mutational burden
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TMB (Tumor Mutational Burden) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1)
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IDH1 mutation • IDH wild-type
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temozolomide
14d
CLINGLIO: LAM561 With RT and TMZ for Adults With Glioblastoma (clinicaltrials.gov)
P2/3, N=144, Active, not recruiting, Laminar Pharmaceuticals | Trial completion date: May 2025 --> Nov 2026 | Trial primary completion date: Oct 2024 --> Jan 2026
Trial completion date • Trial primary completion date
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • MGMT (6-O-methylguanine-DNA methyltransferase)
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MGMT promoter methylation • IDH wild-type
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temozolomide • Minerval (idroxioleic acid)
14d
Trial suspension
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MGMT (6-O-methylguanine-DNA methyltransferase)
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MGMT promoter methylation • IDH wild-type
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Avastin (bevacizumab) • cyclophosphamide • fludarabine IV
14d
Defining Optimal Residual Tumor Volume for Survival in IDH-Wildtype Glioblastoma. (PubMed, World Neurosurg)
An RTV of 1.75 cm3 confers optimal survival benefit in IDH wildtype GBM. A threshold RTV of 1.75 cm3 in methylated and 2.50 cm3 in unmethylated IDH wildtype GBM confers optimal survival benefit. Our findings suggest that RTV may be a more accurate prognostic tool than EOR and could guide surgical decision-making.
Journal
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MGMT (6-O-methylguanine-DNA methyltransferase)
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IDH wild-type
15d
Tumor-associated M2 macrophages shape the cerebrospinal fluid immunoprofile, and the soluble CD163/type I interferon ratio correlates with prognosis in high grade glioma. (PubMed, J Neurooncol)
Elevated sCD163 levels in CSF were positively associated with various TNFSFs and sTNFRs and inversely associated with type 1 IFNs and various ILs, suggesting a dominant influence of tumor associated M2 macrophages on the TME. The sCD163/type I IFN ratio may serve as a potential prognostic indicator in patients with IDH-wildtype glioblastoma.
Retrospective data • Journal
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CD163 (CD163 Molecule) • IFNA1 (Interferon Alpha 1)
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IDH wild-type
17d
Integration and Intersection of Cancer Metabolism with Epigenetic Pathways in Gliomas. (PubMed, Annu Rev Pathol)
Inhibiting IDH mutations with vorasidenib lowers D-2HG and is beneficial to patients. Other drugs like ONC201 and metformin can metabolically suppress oncogenic chromatin states in pediatric gliomas. This dynamic cross talk between metabolism and epigenetics not only underpins tumor biology but also presents opportunities for innovative therapeutic strategies.
Review • Journal
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EGFR (Epidermal growth factor receptor)
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EGFR mutation • IDH wild-type
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metformin • Voranigo (vorasidenib) • Modeyso (dordaviprone)