Relevant bibliographies by topics / Glioma, 2-hydroxyglutarate, IDH, brain tumors

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Glioma, 2-hydroxyglutarate, IDH, brain tumors'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "Glioma, 2-hydroxyglutarate, IDH, brain tumors"

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Iuchi, Toshihiko. "MS2 BRAIN TUMORS AND EPILEPSY." Neuro-Oncology Advances 1, Supplement_2 (2019): ii2. http://dx.doi.org/10.1093/noajnl/vdz039.006.

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Abstract A brain tumor is one of the major causes of epilepsy, and glioma patients frequently exhibit seizures. Epileptic seizure, one of the features of glioma, is also known to be correlated with better outcome of patients. One of the reasons why patients with seizures have a good prognosis is that oligodendroglial tumors tends to cause epilepsy. However, even if limited to glioblastomas, the prognosis with epilepsy is still better than the others. Recently, the association between IDH mutations and epilepsy had been reported. IDH is an enzyme which converts isocitrate to alpha-ketoglutarate
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Nassiri, F., R. Nejad, M. Yasheng, J. Torchia, K. Aldape, and G. Zadeh. "Exploring cellular subpopulations in glioblastoma and matched organoids using single-cell RNA-seq." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, S3 (2018): S14. http://dx.doi.org/10.1017/cjn.2018.298.

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Background: Gliomas are the most common and fatal adult brain tumor with distinct genomic subgroups defined by isocitrate dehydrogenase (IDH) mutation status. Mutations in IDH result in overproduction of the oncometabolite 2-hydroxyglutarate (2HG). The landscape of metabolic changes that define gliomas has not previously been explored. Methods: We performed liquid chromotography-mass spectrometry (LC-MS) to examine over 700 metabolites on 90 fresh-frozen glioma samples (30 IDH-wildtype, 30 IDH-mutant 1p/19q codeleted, 30 IDH-mutant 1p/19q non-codeleted) from our institutional biobank. R and S
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Riviere-Cazaux, Cecile, and Terry Burns. "CLRM-13. INTRAOPERATIVE MICRODIALYSIS: GLIOMA INTELLIGENCE FROM BEHIND ENEMY LINES." Neuro-Oncology Advances 3, Supplement_4 (2021): iv4. http://dx.doi.org/10.1093/noajnl/vdab112.012.

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Abstract INTRODUCTION Gliomas present a formidable challenge for translational progress. Heterogeneity within and between tumors may demand empirically individualized and adaptive paradigms requiring rapid mechanistic feedback. We asked if tumor-associated metabolic biomarkers from glioma extracellular fluid could impart mechanistic “intelligence” reflecting intra- and inter-tumoral heterogeneity. METHODS Five live human gliomas (2 oligos; 2 IDH-WT GBMs; 1 IDH-mutant GBM), were evaluated in situ with high molecular weight (100kDA) intraoperative microdialysis using 3 disparately placed cathete
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Karsy, Michael, Jian Guan, and L. Eric Huang. "Prognostic role of mitochondrial pyruvate carrier in isocitrate dehydrogenase–mutant glioma." Journal of Neurosurgery 130, no. 1 (2018): 56–66. http://dx.doi.org/10.3171/2017.9.jns172036.

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OBJECTIVEGliomas are one of the most common types of primary brain tumors. Recent studies have supported the importance of key genetic alterations, including isocitrate dehydrogenase (IDH) mutations and 1p19q codeletion, in glioma prognosis. Mutant IDH produces 2-hydroxyglutarate from α-ketoglutarate, a key metabolite of the Krebs cycle. The mitochondrial pyruvate carrier (MPC) is composed of MPC1 and MPC2 subunits and is functionally essential for the Krebs cycle. The authors sought to explore the impact of MPC1 and MPC2 expression on patient prognosis.METHODSGenomic and clinical data in pati
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Shi, Diana D., Adam C. Wang, Michael M. Levitt, et al. "DDRE-29. DE NOVO PYRIMIDINE SYNTHESIS IS A TARGETABLE VULNERABILITY IN IDH-MUTANT GLIOMA." Neuro-Oncology Advances 3, Supplement_1 (2021): i12—i13. http://dx.doi.org/10.1093/noajnl/vdab024.051.

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Abstract 70–90% of lower-grade gliomas and secondary glioblastomas harbor gain-of-function mutations in isocitrate dehydrogenase 1 (IDH1), causing overproduction of the oncometabolite (R)-2-hydroxyglutarate [(R)-2HG]. Although inhibitors of mutant IDH enzymes are effective in other cancers, including leukemia, they have shown guarded efficacy in preclinical and clinical brain tumor studies, thus underscoring the need to identify additional therapeutic targets in IDH mutant glioma. We sought to identify tumor-specific metabolic vulnerabilities induced by IDH1 mutations that could be exploited t
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Sarac, S., E. Yilmaz, A. Kayabolen, and T. Bagci Onder. "P19.04.B EXAMINATION OF THE ROLES OF KDM6A AND KDM6B HISTONE DEMETHYLASES IN ISOCITRATE DEHYDROGENASE (IDH) MUTANT GLIOMA." Neuro-Oncology 25, Supplement_2 (2023): ii125. http://dx.doi.org/10.1093/neuonc/noad137.422.

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Abstract Glioma, comprising 80% percent of all malignant brain tumors, is one of the most aggressive and difficult to treat tumors. Isocitrate dehydrogenase (IDH) is an enzyme that catalyzes the oxidative decarboxylation of isocitrate, producing α-ketoglutarate. Most IDH-mutant gliomas have a heterozygous point mutation in IDH1 that causes an arginine-to-histidine substitution at amino acid 132. Mutant IDH enzyme leads to 2-hydroxyglutarate accumulation in cells, inhibiting DNA and histone demethylases and ultimately generating a hypermethylated epigenetic phenotype. Considering that the mutan
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Nguyen, Thanh, Gerd Melkus, Michael Taccone, et al. "IMG-21. PROSPECTIVE PREOPERATIVE DETERMINATION OF ISOCITRATE DEHYDROGENASE MUTATION IN GLIOMAS USING SPECTRAL EDITING MAGNETIC RESONANCE SPECTROSCOPY." Neuro-Oncology 22, Supplement_3 (2020): iii359. http://dx.doi.org/10.1093/neuonc/noaa222.356.

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Abstract BACKGROUND Gliomas are the most common malignant brain tumors in children and adults. A subset of these tumors harbour mutations in the enzyme isocitrate dehydrogenase (IDH) which produces the novel oncometabolite 2-hydroxyglutarate (2HG). In general, patients with an IDH mutant glioma have a longer survival—often necessitating more re-treatment sessions over the span of a patient’s life and surveillance monitoring for tumor recurrence. The need to non-invasively detect early evidence of tumor recurrence is therefore heightened in this unique subset of patients with extended survival.
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Ruiz-Rodado, Victor, Tomohiro Seki, Tyrone Dowdy, et al. "Metabolic Landscape of a Genetically Engineered Mouse Model of IDH1 Mutant Glioma." Cancers 12, no. 6 (2020): 1633. http://dx.doi.org/10.3390/cancers12061633.

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Understanding the metabolic reprogramming of aggressive brain tumors has potential applications for therapeutics as well as imaging biomarkers. However, little is known about the nutrient requirements of isocitrate dehydrogenase 1 (IDH1) mutant gliomas. The IDH1 mutation involves the acquisition of a neomorphic enzymatic activity which generates D-2-hydroxyglutarate from α-ketoglutarate. In order to gain insight into the metabolism of these malignant brain tumors, we conducted metabolic profiling of the orthotopic tumor and the contralateral regions for the mouse model of IDH1 mutant glioma; a
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Reynolds, Nathan, Ashleigh Soedel, Emily Miller, et al. "TMIC-07. MUTANT IDH-MEDIATED SUPPRESSION OF THE TH17 LINEAGE IN GLIOMA; BIOLOGIC IMPACT AND THERAPEUTIC POTENTIAL." Neuro-Oncology 25, Supplement_5 (2023): v279. http://dx.doi.org/10.1093/neuonc/noad179.1073.

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Abstract Great excitement has surrounded the identification of tumor-specific hotspot mutations in IDH1 as they are the first therapeutic targets of low grade gliomas that have been identified in the last several decades. With a low number of viable therapeutic targets, mutations in IDH1 represent new hope in treating these tumors that are invariably recurrent and confer a dismal prognosis in their aggressive forms. Additionally, mutations in IDH1 are tumor-specific suggesting their effective targeting can reduce the collateral damage to the normal brain imparted by standard therapies. Further
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Wenger, Katharina J., Christian Richter, Michael C. Burger, et al. "Non-Invasive Measurement of Drug and 2-HG Signals Using 19F and 1H MR Spectroscopy in Brain Tumors Treated with the Mutant IDH1 Inhibitor BAY1436032." Cancers 12, no. 11 (2020): 3175. http://dx.doi.org/10.3390/cancers12113175.

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Background: BAY1436032 is a fluorine-containing inhibitor of the R132X-mutant isocitrate dehydrogenase (mIDH1). It inhibits the mIDH1-mediated production of 2-hydroxyglutarate (2-HG) in glioma cells. We investigated brain penetration of BAY1436032 and its effects using 1H/19F-Magnetic Resonance Spectroscopy (MRS). Methods: 19F-Nuclear Magnetic Resonance (NMR) Spectroscopy was conducted on serum samples from patients treated with BAY1436032 (NCT02746081 trial) in order to analyze 19F spectroscopic signal patterns and concentration-time dynamics of protein-bound inhibitor to facilitate their ide
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Dissertations / Theses on the topic "Glioma, 2-hydroxyglutarate, IDH, brain tumors"

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Lombardi, Giuseppe. "2-Hydroxyglutarate as a biomarker in glioma patients." Doctoral thesis, Università degli studi di Padova, 2014. http://hdl.handle.net/11577/3423791.

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Background: mutation of IDH1 gene is a prognostic factor and a diagnostic hallmark of gliomas. Mutant IDH1 enzyme can convert α-KG into 2-Hydroxyglutarate (2HG) and mutated gliomas have elevated amounts of intracellular 2HG. Since 2HG is a small molecule it seems possible that it could reach the systemic circulation and to be excreted by urine. And so, we analyzed 2HG concentration in plasma and urine in glioma patients to identify a surrogate biomarker of IDH1 gene mutation. Materials and Methods: All patients had a prior histological confirmation of glioma, a recent brain MRI (within 2 week
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Pirozzi, Christopher James. "Driving Brain Tumorigenesis: Generation and Biological Characterization of a Mutant IDH1 Mouse Model." Diss., 2014. http://hdl.handle.net/10161/9429.

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<p>Despite decades worth of research, glioblastoma remains one of the most lethal cancers. The identification of <italic>IDH1</italic> as a major cancer gene in glioblastoma provides an exceptional opportunity for improving our understanding, diagnostics, and treatment of this disease. In addition to mutations in <italic>IDH1</italic>, recent studies from our laboratory have characterized the genetic landscape of gliomas and have shown the cooperation between IDH1 mutations and other oncogenic alterations such at TP53 mutations. Normally, IDH1 functions in the oxidative decarboxylation of isoc
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Book chapters on the topic "Glioma, 2-hydroxyglutarate, IDH, brain tumors"

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Thien Nhat Tran, Nu. "The Distribution and Significance of IDH Mutations in Gliomas." In Central Nervous System Tumors. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.97380.

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In 2009, the discovery of isocitrate dehydrogenase (IDH) mutations in gliomas is a powerful example of understanding of the relationship between tumor genetics and human diseases. IDHs, catalyze the oxidative decarboxylation of isocitrate to α-ketoglutarate with production of NADH/NADPH, is the key enzymes in the Krebs cycle. IDH mutations, which occur early in gliomagenesis, change the function of the enzymes, causing them to produce 2–hydroxyglutarate, and to not create NADPH. Gliomas with mutated IDH have improved prediction of patient outcomes compared to its with wild-type IDH. Thus, the
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Ahmad, Haroon, and David Schiff. "Diffuse Gliomas (WHO Grade 2–3)." In Neuro-Oncology Compendium for the Boards and Clinical Practice, edited by Maciej M. Mrugala, Na Tosha N. Gatson, Sylvia C. Kurz, Kathryn S. Nevel, and Jennifer L. Clarke. Oxford University PressNew York, 2023. http://dx.doi.org/10.1093/med/9780197573778.003.0004.

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Abstract Grade 2 and grade 3 diffuse gliomas are challenging tumors to treat. They are uncommon, with an incidence rate of 1.35 per 100,000 per year, making them difficult to study. They have a younger median age of onset: 30–40 and 40–60 years old for grade 2 and 3, respectively, making long-term treatment toxicity significant in decision-making. The overwhelming majority of gliomas are sporadic. IDH mutation and 1p/19q co-deletion carry the most weight in prognostication; both are prognostic and predictive. Tumors that are “molecularly equivalent to GBM” and harbor TERT promoter gene mutatio
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Andreatos, Nikolaos, and David M. Peereboom. "Principles of Systemic Therapy in Neuro-Oncology." In Neuro-Oncology Compendium for the Boards and Clinical Practice, edited by Maciej M. Mrugala, Na Tosha N. Gatson, Sylvia C. Kurz, Kathryn S. Nevel, and Jennifer L. Clarke. Oxford University PressNew York, 2023. http://dx.doi.org/10.1093/med/9780197573778.003.0021.

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Abstract Systemic therapy in neuro-oncology refers to the use of any drugs administered systemically rather than locally. The most commonly used drugs are cytotoxic agents, but recent years have seen the advent of targeted therapies such as small-molecule oral compounds and monoclonal antibodies; anti-angiogenic agents; immunotherapy; and, most recently, cellular therapies. Systemic therapies for central nervous system (CNS) malignancies face unique obstacles posed by the blood–brain barrier, although some drugs, such as anti-angiogenic agents and immunotherapies, exert their effects outside o
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