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

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

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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Ventosa, Maria, Padma Kadiyala, Stephen Carney, Maria Castro, and Pedro Lowenstein. "GENE-32. SYNTHETIC LETHAL INTERACTIONS WITH IDH1R132H IN GLIOMA STEM-LIKE CELLS." Neuro-Oncology 21, Supplement_6 (2019): vi104. http://dx.doi.org/10.1093/neuonc/noz175.434.

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Abstract Gliomas are the most frequently diagnosed human primary brain tumors. Mutations in Isocitrate Dehydrogenase (IDH) 1 occur in the vast majority of low grade gliomas and secondary high grade glioblastomas. A single amino acid missense mutation in IDH1 at arginine 132 (R132H) is an early event in tumor development. IDH1R132H leads to the production of the oncometabolite 2-R-2-hydroxyglutarate. However the exact roles played by IDH1R132H in the development and malignant transformation of the tumors remain unclear. Further studies are required to determine optimal therapeutic strategies to

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Gallus, Marco, Darwin Kwok, Senthilnath Lakshmanachetty, Akane Yamamichi, and Hideho Okada. "Immunotherapy Approaches in Isocitrate-Dehydrogenase-Mutant Low-Grade Glioma." Cancers 15, no. 14 (2023): 3726. http://dx.doi.org/10.3390/cancers15143726.

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Low-grade gliomas (LGGs) are slow-growing tumors in the central nervous system (CNS). Patients characteristically show the onset of seizures or neurological deficits due to the predominant LGG location in high-functional brain areas. As a molecular hallmark, LGGs display mutations in the isocitrate dehydrogenase (IDH) enzymes, resulting in an altered cellular energy metabolism and the production of the oncometabolite D-2-hydroxyglutarate. Despite the remarkable progress in improving the extent of resection and adjuvant radiotherapy and chemotherapy, LGG remains incurable, and secondary maligna

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Olson, Ian, Amelia Stepniak, Rebecca Chen, Rafal Chojak, Jason Miska, and Atique Ahmed. "TMIC-53. USE OF CEREBRAL OPEN-FLOW MICROPERFUSION TO IDENTIFY POTENTIAL ONCOMETABOLITE, L-2-HYDROXYGLUTARATE, IN GLIOBLASTOMA CHEMOTHERAPY ADAPTATION." Neuro-Oncology 26, Supplement_8 (2024): viii310. http://dx.doi.org/10.1093/neuonc/noae165.1231.

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Abstract Glioblastoma (GBM) is among the most prevalent and lethal brain tumors, comprising nearly half of all central nervous system malignancies and imparting a median overall survival of only 18-20 months. One major challenge in curing this disease is the limited understanding of how GBM cells biologically respond to treatments like radiotherapy and chemotherapy, including temozolomide (TMZ), in real-time. A significant challenge is observing changes within the tumor interstitial fluid (ISF), which mediates adaptive intercellular signaling between tumor cells and their surrounding tumoral a

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Reynolds, Nathan M., Ashleigh J. Soedel, Ximena Bustamante-Marin, et al. "Abstract 1261: Mutant IDH-mediated suppression of the Th17 lineage in glioma: Biologic impact and therapeutic potential." Cancer Research 83, no. 7_Supplement (2023): 1261. http://dx.doi.org/10.1158/1538-7445.am2023-1261.

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Abstract Great excitement has been generated around the identification of tumor-specific hotspot mutations in isocitrate dehydrogenase I (IDH1) as they are the first potential 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 devastating tumors that are invariably recurrent and confer a dismal prognosis in their most aggressive forms. In addition to their high frequency of mutation in gliomas, mutations in IDH1 are tumor-specific suggesting their

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Tyurina, A. N., A. I. Batalov, N. E. Zakharova, L. M. Fadeeva, D. B. Kalaeva, and I. N. Pronin. "Non-invasive detection of IDH-1 mutation in brain gliomas based on proton MR spectroscopy." Журнал высшей нервной деятельности им. И.П. Павлова 74, no. 1 (2024): 77–84. http://dx.doi.org/10.31857/s0044467724010088.

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Mutations of isocitrate dehydrogenase (IDH) have important prognostic significance for patients with glial brain tumor. The method of proton MR spectroscopy makes it possible to non-invasively determine the metabolic properties of the tumor tissue at the preoperative stage. The aim of this work was to study the possibility of determining the IDH status, by using magnetic resonance spectroscopy (MRS) to detect the 2-hydroxyglutarate (2HG), a metabolic product of the IDH enzyme. We examined 33 patients with glial tumors varying degrees of malignancy (Gr. 2–4), followed by identification of IDH m

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Yanchus, Connor, Kristen Drucker, Thomas Kollmeyer, et al. "EPCO-22. INHERITED POLYMORPHISM IN CHROMOSOME 8Q24 COOPERATES WITH MUTANT IDH1, Trp53 AND ATRX LOSS TO INDUCE LOW-GRADE GLIOMA." Neuro-Oncology 23, Supplement_6 (2021): vi6. http://dx.doi.org/10.1093/neuonc/noab196.021.

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Abstract Establishing causal links between genetic polymorphisms and increased heritable risk of developing brain cancer is a major challenge. The non-coding single nucleotide polymorphism rs55705857 (A &gt;G) is associated with a ~6-fold increased risk to develop IDH-mutant low-grade glioma (LGG). The rs55705857 G allele has a minor allele frequency of only ~5% in the general population but is found in ~40% of patients with IDH-mutant LGG and patients carrying risk-alleles are diagnosed on average 7-12 years earlier than those carrying non-risk A alleles. This makes rs55705857 one of the

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Yalcinkaya, Sedef Sarac, Ebru Yilmaz, Alisan Kayabolen, and Tugba Bagci-Onder. "Abstract 7190: Targeting KDM6A and KDM6B histone demethylases to exploit epigenetic vulnerabilities in IDH mutant gliomas." Cancer Research 85, no. 8_Supplement_1 (2025): 7190. https://doi.org/10.1158/1538-7445.am2025-7190.

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Abstract Gliomas, accounting for 80% of malignant brain tumors, are notably aggressive and may harbor IDH1 mutations, leading to 2-hydroxyglutarate accumulation. This accumulation inhibits DNA and histone demethylases, creating a hypermethylated phenotype. Therefore, understanding and exploiting epigenetic vulnerabilities of IDH1-mutant gliomas may be a powerful therapeutic approach. This study aimed to investigate the roles of lysine demethylases, KDM6A and KDM6B, in the progression of IDH1-mutant gliomas. Using CRISPR/Cas9-mediated gene ablation, we generated IDH1-mutant glioma cell lines (M

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Mortazavi, Armin, Islam Fayed, Muzna Bachani, et al. "OTME-4. IDH mutated gliomas promote epileptogenesis via D-2-hydroxyglutarate dependent mTOR hyperactivation." Neuro-Oncology Advances 3, Supplement_2 (2021): ii14. http://dx.doi.org/10.1093/noajnl/vdab070.055.

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Abstract Epilepsy in the context of brain tumors provides a great burden in these patients, yet mechanisms underlying this process are poorly understood. It has been demonstrated that isocitrate dehydrogenase (IDH) mutations are an independent factor in epileptogenesis in patients with low grade gliomas. Here, using electrographically sorted human cortical tissue from patients with IDH mutated tumor related epilepsy and in vitro cortical cultures, we explore a metabolic paradigm and its impact on increased neuronal excitability. We hypothesize the IDH mutation promotes epileptogenesis through

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Peters, Katherine B. "Targeting Mutant IDH to Treat Low-grade Glioma." Oncology & Haematology 19, no. 2 (2023): 3. http://dx.doi.org/10.17925/ohr.2023.19.2.3.

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Adult-type diffuse low-grade gliomas (LGGs) develop in young adults and represent 5–10% of all primary brain tumours. While patients with LGG can survive longer than those with higher-grade tumours, progression, transformation and, ultimately, mortality occur. Median overall survival for patients with LGGs with multimodal treatment is roughly 13 years from time of diagnosis. Treatment regimens include surgery, radiation therapy and chemotherapy and are based not only on older clinical trials specific to LGG, but also on observations from larger trials in more prevalent high-grade gliomas, such

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Hong, Donghyun, Noriaki Minami, Céline Taglang, et al. "EXTH-46. MRS BASED BIOMARKERS OF IDH1 MUTANT GLIOMA RESPONSE TO THE IDH INHIBITOR BAY-1436032." Neuro-Oncology 23, Supplement_6 (2021): vi173. http://dx.doi.org/10.1093/neuonc/noab196.685.

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Abstract Gliomas are the most prevalent type of brain tumor in the central nervous system. Mutations in the cytosolic enzyme isocitrate dehydrogenase 1 (IDH1) are a common feature of primary low-grade gliomas, catalyzing the conversion of α-ketoglutarate (αKG) to the oncometabolite 2-hydroxyglutarate (2HG), and mutant IDH1 is a therapeutic target for these tumors. Several mutant IDH inhibitors are currently in clinical trials, nonetheless, complementary non-invasive early biomarkers to assess drug delivery and potential therapeutic response are still needed. The goal of this study was therefor

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Rajani, Karishma, Lucas Carlstrom, Joshua Jacobs, et al. "BIMG-20. METABOLIC BIOMARKERS IN MICRODIALYSATE OF IDH-1 MUTANT TUMORS." Neuro-Oncology Advances 3, Supplement_1 (2021): i5. http://dx.doi.org/10.1093/noajnl/vdab024.019.

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Abstract Glioblastoma (GBM) is a common deadly malignant brain cancer of the central nervous system, with a median survival of 12–15 months. Scientific advancements are lacking in developing effective therapies for both primary GBM, as well as secondary GBMs, that typically originate as malignant transformation of lower-grade isocitrate dehydrogenase (IDH) 1-mutant tumors. The unique metabolomic profile of IDH1-mutant tumors presents opportunities to develop biomarker signatures of therapeutic efficacy. Microdialysis is an extracellular fluid sampling collection technique utilizing a perfused

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Tamura, Kaoru, Yaeko Furuhashi, Motoki Inaji, et al. "NI-06 MOLECULAR DIAGNOSIS, 11C-METHIONINE UPTAKE AND PROGNOSIS IN GRADE 2 AND 3 GLIOMAS." Neuro-Oncology Advances 1, Supplement_2 (2019): ii26. http://dx.doi.org/10.1093/noajnl/vdz039.119.

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Abstract OBJECT The revised 2016 WHO Classification of Tumours of the Central Nervous System incorporates genetic alterations into the classification system, with the goal of creating more homogenous disease categories with greater prognostic value. In this study, we reclassified 103 consecutive lower grade gliomas using the revised 2016 WHO classification and examined for 11C-methionine uptake and prognosis. METHODS 103 consecutive lower grade glioma patients (Grade 2 in 41 patients, Grade 3 in 62 patients) treated at Tokyo Medical and Dental University Hospital from 2000 to 2018 were include

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Kushnirsky, Marina, Sunitha Thakur, Matthias Karajannis, et al. "NIMG-57. NON-INVASIVE DIAGNOSIS OF IDH-MUTANT BRAINSTEM GLIOMAS." Neuro-Oncology 24, Supplement_7 (2022): vii176—vii177. http://dx.doi.org/10.1093/neuonc/noac209.675.

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Abstract INTRODUCTION Treatment of brainstem tumors is often initiated without a tissue diagnosis due to the risk of biopsy. A subset of brainstem gliomas harbor an isocitrate dehydrogenase 1/2 (IDH) mutation, which predicts response to alkylator chemotherapy and IDH inhibitors; non-invasive diagnostic tests are needed to identify these mutations. METHODS We identified a cohort of patients with IDH-mutant brainstem gliomas through chart review of patients who underwent magnetic resonance spectroscopy (MRS) and/or brain biopsy. IDH mutation was established by biopsy, presence of a 2-hydroxyglut

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Schaff, Lauren, John Fortunato, Christian Grommes, et al. "Phase II trial of combination pembrolizumab, olaparib, and temozolomide for patients with recurrent glioma." Journal of Clinical Oncology 41, no. 16_suppl (2023): TPS2087. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.tps2087.

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TPS2087 Background: Diffuse gliomas are primary brain tumors characterized by substantial morbidity and mortality. Standard treatment includes maximal safe surgical resection followed by combination radiation and chemotherapy. Despite aggressive treatment, diffuse gliomas inevitably recur. Alkylating agents, and in particular temozolomide, play an important role in the treatment of gliomas, resulting in single-strand DNA breakages which require PARP activity for detection and repair. Gliomas with mutations in isocitrate dehydrogenase ( IDH) 1 or 2 have an accumulation of 2-hydroxyglutarate (2H

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Tamura, Kaoru, Motoki Inaji, Daisuke Kobayashi, et al. "NI-10 Reclassification of diffuse gliomas based on molecular diagnosis -evaluation of methionine uptake and treatment outcome-." Neuro-Oncology Advances 3, Supplement_6 (2021): vi19. http://dx.doi.org/10.1093/noajnl/vdab159.072.

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Abstract Object: The revised 2016 WHO Classification of Tumours of the Central Nervous System incorporates genetic alterations into the classification system, with the goal of creating more homogenous disease categories with greater prognostic value. In this study, we reclassified diffuse gliomas with molecular diagnosis and examined for 11C-methionine uptake and prognosis. Methods. 182 diffuse glioma patients (Grade II in 42 patients, Grade III in 61 patients, Grade IV in 77 patients) treated at Tokyo Medical and Dental University Hospital from 2000 to 2018 were included in this study. The ID

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Fritah, S., A. Cano-Galiano, R. Toth, et al. "P02.18.B INTEGRATIVE OMICS ANALYSIS OF IDH1 MUTANT GLIOMA PATIENTS REVEALS ALTERATIONS IN BUTYRATE METABOLISM." Neuro-Oncology 25, Supplement_2 (2023): ii33—ii34. http://dx.doi.org/10.1093/neuonc/noad137.103.

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Abstract BACKGROUND Mutations in isocitrate dehydrogenase (IDH) 1 or 2 define glioma classification and determine the biology of these tumors. Although IDH is an essential enzyme in the cellular metabolism, powerful genome-wide analyses focus mostly at the genetic and epigenetic levels, while differences between distinct glioma entities at the proteomics, metabolomics, and functional levels are still poorly understood. Here, we provide an integrative multi-omics analysis of glioma patients to reveal metabolomic vulnerabilities of gliomas stratified by IDH mutation. MATERIAL AND METHODS We perf

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Kim, Lauren, Henk De Feyter, Robin de Graaf, et al. "NIMG-105. DEUTERIUM METABOLIC IMAGING (DMI) DETECTS A LARGER WARBURG EFFECT IN HIGH-GRADE BRAIN TUMORS AND IN IDH WILD TYPE GLIOMAS." Neuro-Oncology 24, Supplement_7 (2022): vii189. http://dx.doi.org/10.1093/neuonc/noac209.723.

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Abstract BACKGROUND The Warburg Effect (WE) is a metabolic change in which tumors favor glycolysis over oxidative phosphorylation and has been linked to cancer aggressiveness. Mutations in the isocitrate dehydrogenase (IDH) genes in gliomas are associated with improved outcomes. We deployed a magnetic resonance (MR) spectroscopic imaging technique coined Deuterium Metabolic Imaging (DMI) to measure the WE in multiple brain tumor types. METHODS Twenty-one patients underwent DMI, acquired on a Bruker 4T MR scanner after oral administration of 0.75g/kg of deuterated glucose. The WE was defined as

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Kit, O. I., D. I. Vodolazhsky, E. E. Rostorguev, D. H. Porksheyan, and S. B. Panina. "The role of micro-RNA in the regulation of signal pathways in gliomas." Biomeditsinskaya Khimiya 63, no. 6 (2017): 481–98. http://dx.doi.org/10.18097/pbmc20176306481.

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Gliomas are invasive brain tumors with high rates of recurrence and mortality. Glioblastoma multiforme (GBM) is the most deadly form of glioma with nearly 100% rate of recurrence and unfavorable prognosis in patients. Micro-RNAs (miR) are the class of wide-spread short non-coding RNAs that inhibit translation via binding to the mRNA of target genes. The aim of the present review is to analyze recent studies and experimental results concerning aberrant expression profiles of miR, which target components of the signaling pathways Hedgehog, Notch, Wnt, EGFR, TGFb, HIF1a in glioma/glioblastoma. Pa

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Kim, Lauren, Henk De Feyter, Robin de Graaf, et al. "NEIM-11 DEUTERIUM METABOLIC IMAGING (DMI) DETECTS A LARGER WARBURG EFFECT IN HIGH-GRADE BRAIN TUMORS AND IN IDH WILD TYPE GLIOMAS." Neuro-Oncology Advances 5, Supplement_3 (2023): iii16. http://dx.doi.org/10.1093/noajnl/vdad070.060.

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Abstract BACKGROUND The Warburg Effect (WE) is a metabolic change in which tumors favor glycolysis over oxidative phosphorylation and has been linked to cancer aggressiveness. Mutations in the isocitrate dehydrogenase (IDH) genes in gliomas are associated with improved outcomes. We deployed a magnetic resonance (MR) spectroscopic imaging technique coined Deuterium Metabolic Imaging (DMI) to measure the WE in multiple brain tumor types. METHODS Twenty-one patients underwent DMI, acquired on a Bruker 4T MR scanner after oral administration of 0.75g/kg of deuterated glucose. The WE was defined as

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McClellan, Brandon, Ali Dabaja, Kaushik Banerjee, et al. "IMMU-19. MUTANT ISOCITRATE DEHYDROGENASE 1 IN GLIOMA CAUSES A REDUCTION IN ADENOSINERGIC PATHWAY SIGNALING WITHIN THE TUMOR MICROENVIRONMENT." Neuro-Oncology 25, Supplement_5 (2023): v145. http://dx.doi.org/10.1093/neuonc/noad179.0551.

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Abstract Glioma is one of the most aggressive cancers and represents approximately 80% of malignant brain tumors. The majority of CNS World Health Organization (WHO) grades 2-3 gliomas and a subset of high-grade gliomas (CNS WHO grade 4) harbor mutated isocitrate dehydrogenase 1 (IDH1R132H; mIDH1). Mutant IDH1 results in the accumulation of 2-hydroxyglutarate (2HG) which elicits profound changes in the glioma transcriptome/biology. Consequently, mIDH1 glioma patients have a significantly increased median survival compared to wildtype IDH1 patients. Recent data from our lab showed that mIDH1 gl

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Cox, Thomas J. R., Eren Ozcagli, Giuseppe Schettino, and Lisiane B. Meira. "Abstract B108: NUDT5 inhibition differentially affects IDH1-Wildtype and Mutant high-grade glioma to induce NAD+ independent radiosensitization and anti-proliferative effects." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): B108. http://dx.doi.org/10.1158/1535-7163.targ-23-b108.

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Abstract Adult-type diffuse gliomas are aggressive brain cancers. The widespread standard treatment for these high-grade gliomas (HGG) is the Stupp Protocol, consisting of maximal safe surgical resection followed by concurrent chemoradiotherapy. However, since the Stupp Protocol, no significant therapeutic advances have been as widely and easily adopted, halting improvements in HGG patient survival. Therefore, identifying new drug targets or treatments that enhance the Stupp Protocol would result in therapeutic benefit. HGG are classified by distinct genetic and metabolic alterations; the most

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Chen, Ricky, Vijay M. Ravindra, Adam L. Cohen, et al. "Molecular features assisting in diagnosis, surgery, and treatment decision making in low-grade gliomas." Neurosurgical Focus 38, no. 3 (2015): E2. http://dx.doi.org/10.3171/2015.1.focus14745.

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The preferred management of suspected low-grade gliomas (LGGs) has been disputed, and the implications of molecular changes for medical and surgical management of LGGs are important to consider. Current strategies that make use of molecular markers and imaging techniques and therapeutic considerations offer additional options for management of LGGs. Mutations in the isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) genes suggest a role for this abnormal metabolic pathway in the pathogenesis and progression of these primary brain tumors. Use of magnetic resonance spectroscopy can provide preoper

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Sankowski, R., M. Friedrich, L. Bunse, H. H. Heiland, M. Platten, and M. Prinz. "KS01.6.A Comparative analysis of the immune compartment in human glioblastoma and IDH-mutant WHO grade 4 astrocytoma reveals profound differences in microglia phenotypes." Neuro-Oncology 23, Supplement_2 (2021): ii4. http://dx.doi.org/10.1093/neuonc/noab180.010.

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Abstract BACKGROUND Glioblastoma (GBM) are the most common primary brain tumors. If untreated the average survival is around 12–18 months. Unfortunately, despite extensive research efforts, the therapeutic options remain limited. One major aspect complicating therapeutic development is an immunosuppressive tumor microenvironment. Isocitrate dehydrogenase (IDH)-mutant, WHO grade 4 astrocytomas appear histologically indistinguishable from GBM, but show significantly longer survival times. IDH mutations lead to changes in the tumor microenvironment with accrual of the neometabolite R-2-hydroxyglu

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Skvortsova, T. Yu, Zh I. Savintseva, A. F. Gurchin, and A. I. Kholyavin. "Can the metabolic characteristics of diffuse glioma on <sup>11</sup>C-methionine PET/CT serve as a marker of its IDH status? Cross sectional study." Diagnostic radiology and radiotherapy 15, no. 1 (2024): 35–45. http://dx.doi.org/10.22328/2079-5343-2024-15-1-35-45.

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INTRODUCTION: Since 2016, molecular markers, in particular, mutations in isocitrate dehydrogenase (IDH) 1 and 2, have been introduced as a classifying feature of cerebral gliomas that provided superior prognostication. The search for non-invasive biomarkers of the molecular profile of gliomas is necessary to improve the quality of preoperative diagnostics, identify patients with good and poor prognosis and determine treatment tactics.OBJECTIVE: Was to study the relationship between the IDH genotype of diffuse cerebral gliomas and metabolic biomarkers according to the results of PET/CT with [11

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Horbinski, Craig, Louis Burt Nabors, Jana Portnow, et al. "NCCN Guidelines® Insights: Central Nervous System Cancers, Version 2.2022." Journal of the National Comprehensive Cancer Network 21, no. 1 (2023): 12–20. http://dx.doi.org/10.6004/jnccn.2023.0002.

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The NCCN Guidelines for Central Nervous System (CNS) Cancers focus on management of the following adult CNS cancers: glioma (WHO grade 1, WHO grade 2–3 oligodendroglioma [1p19q codeleted, IDH-mutant], WHO grade 2–4 IDH-mutant astrocytoma, WHO grade 4 glioblastoma), intracranial and spinal ependymomas, medulloblastoma, limited and extensive brain metastases, leptomeningeal metastases, non–AIDS-related primary CNS lymphomas, metastatic spine tumors, meningiomas, and primary spinal cord tumors. The information contained in the algorithms and principles of management sections in the NCCN Guideline

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Coffee, Elizabeth, Katherine Panageas, Robert Young, et al. "CTNI-55. THE CDK4/6 INHIBITOR ABEMACICLIB IN PATIENTS WITH RECURRENT MENINGIOMA AND OTHER PRIMARY CNS TUMORS." Neuro-Oncology 23, Supplement_6 (2021): vi72—vi73. http://dx.doi.org/10.1093/neuonc/noab196.280.

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Abstract BACKGROUND Medical therapies for recurrent brain tumors are limited. Abemaciclib is a small molecule CDK4/6 inhibitor that has demonstrated antitumor activity in multiple cancer types and crosses the blood-brain barrier. METHODS We conducted a phase II trial of single-agent abemaciclib in patients with recurrent primary brain tumors utilizing a novel CNS basket trial design with multiple tumor types accrued to separate cohorts including patients with recurrent IDH-wildtype gliomas (Cohort A), any recurrent gliomas requiring cytoreductive surgery (Cohort B), and any other recurrent pri

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Gupta, Pravesh, Minghao Dang, Shivangi Oberai, et al. "Abstract 669: Immunophenotyping of human brain tumors reveals myeloid cell mediated anti-glioma axis." Cancer Research 83, no. 7_Supplement (2023): 669. http://dx.doi.org/10.1158/1538-7445.am2023-669.

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Abstract Gliomas are recalcitrant brain tumors. Differential tumor immune reactivity contributes to survival advantage of isocitrate dehydrogenase-mutant (IDHmut) over wild-type (IDHwt) gliomas. Despite this correlative pattern of immunity and survival, only a limited view of a highly complex immune contexture across IDH mutation classified gliomas is known. Herein, we present an unprecedented view of myeloid and lymphoid cell type diversity by single cell RNA sequencing and spectral cytometry-based interrogation of tumor-associated leukocytes from fifty-five IDH stratified primary and recurre

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Taglang, Celine, Georgios Batsios, Meryssa Tran, et al. "BIMG-05. TO BE OR NOT TO BE GLYCOLYTIC: DEUTERATED GLUCOSE-BASED ASSESSMENT OF THE WARBURG EFFECT ALLOWS NON-INVASIVE IMAGING OF TUMOR BURDEN AND TREATMENT RESPONSE IN MUTANT IDH GLIOMAS IN VIVO." Neuro-Oncology Advances 3, Supplement_1 (2021): i1—i2. http://dx.doi.org/10.1093/noajnl/vdab024.004.

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Abstract The Warburg effect, characterized by elevated glucose uptake and flux to lactate, is a metabolic hallmark of cancer. Recent studies have identified deuterium 2H-magnetic resonance spectroscopy (MRS) using 6,6’-2H-glucose as a novel method of imaging the Warburg effect in high-grade primary glioblastomas (GBMs). However, its utility for imaging low-grade gliomas has not been tested. The goal of this study was to determine whether 6,6’-2H-glucose can be used for imaging tumor burden and treatment response in mutant isocitrate dehydrogenase (IDHmut) low-grade gliomas in vivo. We examined

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Eisele, A., M. Mastall, M. Weller, and P. Roth. "P06.03.A EXPLORING THE THERAPEUTIC EFFICACY OF CHLOROQUINE AND HYDROXYCHLOROQUINE IN IDH-WILDTYPE AND IDH-MUTANT GLIOMA." Neuro-Oncology 26, Supplement_5 (2024): v44. http://dx.doi.org/10.1093/neuonc/noae144.140.

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Abstract BACKGROUND Within the treatment of the most common and aggressive brain tumors - gliomas - the last decades have been characterized by an enormously high rate of failed and cost-intensive drug trials. Repurposing established medications for the treatment of cancer has the advantage of faster availability as well as cost-effectiveness. Chloroquine (CQ) and hydroxychloroquine (HCQ) are approved medications for the treatment of rheumatologic diseases and malaria and have gained attention in recent years due to evidence of potential anti-tumor efficacy in various cancer types. The data av

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Garcia, Diogo, Hannah Brown, Mark Jentoft, et al. "Intra-operative desorption-electrospray ionization mass-spectrometry for real-time diagnosis, margin assessment, and maximization of brain cancer resection." Journal of Clinical Oncology 41, no. 16_suppl (2023): 2071. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.2071.

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2071 Background: Despite advances in our understanding of brain cancer, the ability to discern between infiltrated and non-infiltrated tissue with current adjuncts, remains elusive. Isocitrate dehydrogenase (IDH) mutation is unique to IDH-mut glioma cells and can be used as a surrogate for tumor infiltration. Further, emerging evidence has shown unique signatures in brain cancer lipidomic profiling, with lipid metabolism playing a key role in brain cancer biology. Here, we aimed to evaluate the impact of desorption electrospray ionization-mass spectrometry (DESI-MS) as a near real-time method

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Bhattacharya, Abhishek, and Anand Kornepati. "Abstract 1133: Molecular evolution patterns in primary versus recurrent adult gliomas: A multi-institutional study from Project GENIE." Cancer Research 85, no. 8_Supplement_1 (2025): 1133. https://doi.org/10.1158/1538-7445.am2025-1133.

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Abstract Introduction: Gliomas are the most common primary malignant brain tumors in adults, with high recurrence rates despite multimodal treatment. While previous multi-institutional genomic studies have revealed molecular differences between primary and recurrent tumors, the AACR Project GENIE dataset provides another valuable resource to investigate these distinctions. Methods: We analyzed 8, 959 adult glioma cases from Project GENIE v16.1 (2024), selecting cases with complete mutation and copy number alteration (CNA) data. Tumors were stratified by Isocitrate dehydrogenase (IDH) mutation

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Kim, Hyunhee, Ka Young Lim, Jin Woo Park, et al. "Sporadic and Lynch syndrome-associated mismatch repair-deficient brain tumors." Laboratory Investigation 102, no. 2 (2021): 160–71. http://dx.doi.org/10.1038/s41374-021-00694-3.

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AbstractMismatch repair-deficient (MMRD) brain tumors are rare among primary brain tumors and can be induced by germline or sporadic mutations. Here, we report 13 MMRD-associated (9 sporadic and 4 Lynch syndrome) primary brain tumors to determine clinicopathological and molecular characteristics and biological behavior. Our 13 MMRD brain tumors included glioblastoma (GBM) IDH-wildtype (n = 9) including 1 gliosarcoma, astrocytoma IDH-mutant WHO grade 4 (n = 2), diffuse midline glioma (DMG) H3 K27M-mutant (n = 1), and pleomorphic xanthoastrocytoma (PXA) (n = 1). Next-generation sequencing using

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Rathore, Saima, Suyash Mohan, Spyridon Bakas, et al. "Multi-institutional noninvasive in vivo characterization of IDH, 1p/19q, and EGFRvIII in glioma using neuro-Cancer Imaging Phenomics Toolkit (neuro-CaPTk)." Neuro-Oncology Advances 2, Supplement_4 (2020): iv22—iv34. http://dx.doi.org/10.1093/noajnl/vdaa128.

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Abstract Background Gliomas represent a biologically heterogeneous group of primary brain tumors with uncontrolled cellular proliferation and diffuse infiltration that renders them almost incurable, thereby leading to a grim prognosis. Recent comprehensive genomic profiling has greatly elucidated the molecular hallmarks of gliomas, including the mutations in isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2), loss of chromosomes 1p and 19q (1p/19q), and epidermal growth factor receptor variant III (EGFRvIII). Detection of these molecular alterations is based on ex vivo analysis of surgically res

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Wen, Patrick, Macarena de la Fuente, Priya Kumthekar, et al. "CTIM-19. A PHASE 1, SAFETY LEAD-IN AND RANDOMIZED, OPEN-LABEL, PERIOPERATIVE STUDY OF VORASIDENIB COMBINED WITH PEMBROLIZUMAB IN RECURRENT OR PROGRESSIVE ENHANCING IDH-1 MUTANT GLIOMA: TRIAL IN PROGRESS." Neuro-Oncology 26, Supplement_8 (2024): viii89. http://dx.doi.org/10.1093/neuonc/noae165.0352.

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Abstract BACKGROUND Vorasidenib (VOR) is an oral, brain-penetrant dual inhibitor of isocitrate dehydrogenase 1/2 mutant (mIDH1/2) enzymes. VOR is being investigated in a phase 3 study in residual or recurrent grade 2 non-enhancing gliomas, in which interim analysis showed VOR significantly improved progression-free survival and delayed time to next intervention. A prior neoadjuvant perioperative study in recurrent, non-enhancing grade 2/3 gliomas showed that VOR treatment was associated with interferon signal activation and increased T-cell infiltration, suggesting 2-hydroxyglutarate suppressi

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Shrestha, Roshani, Simit Sapkota, Abish Adhikari, Subhas Pandit, Anjani Jha, and Prakriti Karki. "CLRM-05 ADAPTATION OF NEW CLASSIFICATION OF ASTROCYTOMA IN LOW AND MIDDLE INCOME COUNTRY- HOW SMOOTH IS THE ROAD AHEAD?" Neuro-Oncology Advances 5, Supplement_3 (2023): iii8. http://dx.doi.org/10.1093/noajnl/vdad070.028.

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Abstract BACKGROUND The 2021 WHO CNS 5 classification made major changes with integration of immunohistochemistry, molecular profiling and sequencing in addition to histopathology to classify brain tumors. IDH mutation is mainstay for diagnosis of low grade glioma and 1p/19q testing required only to confirm oligodendroglioma but not in all cases. This integrated approach has favored prognosis, and diagnosis of disease as well as prediction of response to therapy. METHODS A retrospective study was conducted to analyze the molecular alterations in patients diagnosed with astrocytoma in 2021 in K

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Hollon, Todd, Cheng Jiang, Mustafa Nasir-Moin, et al. "NIMG-30. AI-BASED MOLECULAR CLASSIFICATION OF DIFFUSE GLIOMAS USING RAPID, LABEL-FREE OPTICAL HISTOLOGY." Neuro-Oncology 24, Supplement_7 (2022): vii169. http://dx.doi.org/10.1093/neuonc/noac209.648.

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Abstract INTRODUCTION Molecular classification has transformed the management of brain tumors by enabling more accurate prognostication and personalized treatment. Access to timely molecular diagnostic testing for brain tumor patients is limited, complicating surgical and adjuvant treatment and obstructing clinical trial enrollment. OBJECTIVE We aim to develop a rapid (&lt; 90 seconds), AI-based diagnostic screening system that can provide molecular classification of diffuse gliomas and report its use in a prospective, multicenter, international clinical trial of diffuse glioma patients (n

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Mellinghoff, Ingo K., Katherine B. Peters, Timothy Francis Cloughesy, et al. "Vorasidenib (VOR; AG-881), an inhibitor of mutant IDH1 and IDH2, in patients (pts) with recurrent/progressive glioma: Updated results from the phase I non-enhancing glioma population." Journal of Clinical Oncology 38, no. 15_suppl (2020): 2504. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.2504.

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2504 Background: Isocitrate dehydrogenase 1 and 2 mutations (m IDH1/2) occur in approximately 70% and 4% of low-grade gliomas (LGGs), respectively, promoting oncogenesis via increased production of D-2-hydroxyglutarate. In this ongoing phase 1 trial, VOR, a potent, oral, reversible, brain-penetrant, first-in-class dual inhibitor of mIDH1/2, is being evaluated in advanced m IDH1/2 solid tumors, including gliomas. Safety and preliminary results were presented previously (Mellinghoff et al., J Clin Oncol 2018). Here, we report updated data for the non-enhancing glioma pt population. Methods: Pts

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Banerjee, Kaushik, Felipe Nunez, Anzar Mujeeb, et al. "TMIC-79. IDH1-R132H REWIRES AUTOPHAGY IN THE GLIOMA MICROENVIRONMENT TO FACILITATE TUMOR PROGRESSION AND RESPONSE TO RADIATION." Neuro-Oncology 26, Supplement_8 (2024): viii316. http://dx.doi.org/10.1093/neuonc/noae165.1256.

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Abstract Gliomas are primary brain tumors with a poor prognosis. IDH1R132H exhibits a gain of function mutation leading to 2-hydroxyglutarate (2HG) production. We previously demonstrated, 2-HG mediated epigenetic rewiring is associated with better prognosis and its presence impacts several cellular functions including immune responses and enhanced DNA-damage response in IDH1R132H gliomas harboring p53 and ATRX loss-of-function mutations. Also, IDH1R132H elicits metabolic reprogramming which implies that IDH1R132H could modify the energetic state of gliomas with consequences in tumor biology an

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Parthasarathy, Akhila, Antje Arnold, Charles Eberhart, and Eric Raabe. "EXTH-15. MULTI-FACETED INHIBITION OF TET PATHWAY WITH CELL-PERMEABLE 2HG AND BOBCAT 339 REDUCES PROLIFERATION AND INDUCES APOPTOSIS IN DIPG." Neuro-Oncology 23, Supplement_6 (2021): vi166. http://dx.doi.org/10.1093/neuonc/noab196.654.

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Abstract Diffuse Intrinsic Pontine Glioma (DIPG) is one of the worst forms of pediatric brain tumors, with a 100% mortality-rate. A prominent mutation observed in them is a lysine to methionine change in histone3 which causes trapping of the repressive-chromatin-complex, leading to genome-level hypomethylation, affecting global epigenetic-regulation. Ten-Eleven Translocation (TET) proteins are alpha-ketoglutarate (α-KG) dependent dioxygenases that mediate the conversion of 5-methylcytosine to 5-hydroxymethylcytosine (5hmC), a key-step in removing DNA methylation-marks. We previously identified

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Galldiks, Norbert, Marcus Unterrainer, Natalie Judov, et al. "Photopenic defects on O-(2-[18F]-fluoroethyl)-L-tyrosine PET: clinical relevance in glioma patients." Neuro-Oncology 21, no. 10 (2019): 1331–38. http://dx.doi.org/10.1093/neuonc/noz083.

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Abstract Background O-(2-[18F]-fluoroethyl)-L-tyrosine (FET) PET has a sensitivity of more than 90% to detect gliomas. In the remaining small fraction of gliomas without increased tracer uptake, some tumors even show photopenic defects whose clinical significance is unclear. Methods Glioma patients with a negative FET PET scan prior to neuropathological confirmation were identified retrospectively. Gliomas were rated visually as (i) having indifferent FET uptake or (ii) photopenic, if FET uptake was below background activity. FET uptake in the area of signal hyperintensity on the T2/fluid atte

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