Comparison of gene expression profiles of anaplastic glioma with or without the mutated IDH1/2 gene
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE52942 | GEO | 2013/12/04
SECONDARY ACCESSION(S): PRJNA230506
REPOSITORIES: GEO
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Project description:The aim of ths study is to compare global methylation status between 1) IDH1 mutant and IDH1/2 wild-type glioblastoma tumorsphere cells and 2) MGG152 (IDH1 mutant) with DMSO and IDH1 inhibitor treatment. Genome wide DNA methylation profiling of patient derived glioblastoma tumorsphere and HT1080 cells. The Illumina Infinium Human DNA methylation Beadchip450 was used to obtain DNA methylation profiles. Bisulphite converted DNA from the 10 samples and one control were hybridised to the Illumina Infinium Human Methylation Beadchip450. Please note that the MGG (in the sample title) represents patient-derived MGH glioblastoma cell lines. Regarding MGG152 samples, sample no.1 is low passage number and used for comparison between IDH1 mt and wild-type. Sample no. 2-4 were used for assessing DNA methylation change after short term or long term IDH1 inhibiting treatment.
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Project description:The discovery of the IDH1 R132H (IDH1 mut) mutation in low-grade glioma and the associated change in function of the IDH1 enzyme has increased the interest in glioma metabolism. In an earlier study, we found that changes in expression of genes involved in the aerobic glycolysis and the TCA-cycle are associated with IDH1 mut. Here we apply proteomics to FFPE samples of diffuse gliomas with or without IDH1 mutations, in order to map changes in protein levels associated with this mutation. We observed significant changes in the enzyme abundance associated with aerobic glycolysis, glutamate metabolism and the TCA-cycle in IDH1 mut gliomas. Specifically, the enzymes involved in the metabolism of glutamate, lactate and enzymes involved in the conversion of α-ketoglutarate were increased in IDH1 mut gliomas. In addition, the bicarbonate transporter (SLC4A4) was increased in IDH1 mut gliomas, supporting the idea that a mechanism preventing intracellular acidification is active. We also found that enzymes that convert proline, valine, leucine and isoleucine into glutamate were increased in IDH1 mut glioma. We conclude that in IDH1 mut glioma metabolism is rewired (increased input of lactate and glutamate) to preserve TCA cycle activity in IDH1 mut gliomas.
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Project description:The discovery of the IDH1 R132H (IDH1 mut) mutation in low-grade glioma and the associated change in function of the IDH1 enzyme has increased the interest in glioma metabolism. In an earlier study, we found that changes in expression of genes involved in the aerobic glycolysis and the TCA-cycle are associated with IDH1 mut. Here we apply proteomics to FFPE samples of diffuse gliomas with or without IDH1 mutations, in order to map changes in protein levels associated with this mutation. We observed significant changes in the enzyme abundance associated with aerobic glycolysis, glutamate metabolism and the TCA-cycle in IDH1 mut gliomas. Specifically, the enzymes involved in the metabolism of glutamate, lactate and enzymes involved in the conversion of α-ketoglutarate were increased in IDH1 mut gliomas. In addition, the bicarbonate transporter (SLC4A4) was increased in IDH1 mut gliomas, supporting the idea that a mechanism preventing intracellular acidification is active. We also found that enzymes that convert proline, valine, leucine and isoleucine into glutamate were increased in IDH1 mut glioma. We conclude that in IDH1 mut glioma metabolism is rewired (increased input of lactate and glutamate) to preserve TCA cycle activity in IDH1 mut gliomas.
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Project description:Mutations in the IDH1 and IDH2 genes encoding isocitrate dehydrogenases are frequent in human glioblastomas1 and cytogenetically normal acute myeloid leukemias (AML)2. These alterations are gain-of-function mutations in that they drive the synthesis of the M-bM-^@M-^\oncometaboliteM-bM-^@M-^] R-2-hydroxyglutarate (2HG)3. It remains unclear how IDH1 and IDH2 mutations modify myeloid cell development and promote leukemogenesis. Here we report the characterization of conditional knock-in mice in which the most common IDH1 mutation, Idh1-R132H, is inserted into the endogenous murine Idh1 locus and is expressed in cells of the hematopoietic (Vav-KI) or more specifically in cells of the myeloid (LysM-KI) lineage. These mutants show increased numbers of early hematopoietic progenitors and develop splenomegaly and anemia with extramedullary hematopoiesis, suggesting a dysfunctional bone marrow niche. Furthermore, LysM-KI cells exhibit both hypermethylated histones and changes to DNA methylation similar to those observed in human IDH1/2-mutant AML. Thus, our study is the first to describe the generation of conditional Idh1-R132H-KI mice. Furthermore, our study is also the first report showing the induction of a leukemic DNA methylation signature in a modeled system and sheds light on the mechanistic links between IDH1 mutation and human AML. DNA methylation profiling in LSK cells from IDH1-R132H knock-in mice vs. control mice
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Project description:Ollier disease and Maffucci syndrome are non-hereditary skeletal disorderscharacterized by multiple enchondromas (Ollier disease) combined with spindle cellhemangiomas (Maffucci syndrome). Somatic heterozygous IDH1 (R132C and R132H) orIDH2 (R172S) mutations were found in 87% of enchondromas, benign cartilage tumors,as well as in 70% of spindle cell hemangiomas, benign vascular lesions. In total, 35 of 43(81%) patients with Ollier disease and 10 of 13 (77%) patients with Maffucci syndromecarried IDH1 (98%) or rarely IDH2 (2%) mutations in their tumors. Fourteen patientswith multiple tumors at different anatomic locations displayed identical mutations inseparate lesions. Since in other tumor types the presence of an IDH1 mutation is strongly associated withhypermethylation 26, 27, we assessed whether there was a difference in methylation patternof enchondromas with (n = 8) and without (n = 4) IDH1 mutations detactable at Sangersequencing. Methylation and expressionprofiling showed that IDH1 mutations in cartilage tumors are associated withhypermethylation and downregulation of the expression of several genes. Total 12 samples which includes 8 enchondromas with IDH1 mutation (4 Ollier enchondromas, 2 Maffucci enchondromas and 2 solitary enchondromas) and 4 enchondromas (1 Ollier enchondroma, 3 solitary enchondromas) without IDH1 or IDH2 mutations were used. Of these 4 enchondromas without IDH1 mutation, one had R132G IDH1 mutated cells present in the subpopulation, below the threshold level of Sanger sequencing. Bisulfite treatment was performed using EZ DNA Methylation™ Kit (ZymoResearch, Orange, CA). Bisulphite converted DNA was then hybridized to IlluminaHumanMethylation27 BeadChip (Illumina Inc., San Diego, CA) by followingmanufacturer’s instructions. Infinium Unsupervised clustering analysis was performed 25 using the Ward’s clustering algorithm based on Euclidian distance. The 2000 most variable CpG sites (excluding those on the X and Y chromosomes) were used in the clustering analysis.
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