Similar Datasets
Project description:Immortalized human astrocytes were stably transfected to express IDH1 R132H. These cells were treated with 1uM ATRA
2024-04-01 | GSE252527 | GEO
Project description:Human acute myeloid leukemia HL60 cells were transduced with IDH1-WT or IDH1-R132H, and corresponding sub-clones were generated by FACS. In a first series of experiments, cells expressing wt and mutant IDH1were treated with either 1µM all-trans retinoic acid (ATRA) or with vehicle (DMSO) for 24 hrs, resulting in 4 groups of samples (WT-CTRL, WT-ATRA, Mutant-CTRL, Mutant-ATRA). In a second series of assays, WT-IDH1 cells were pre-treated for 2 days with either 100 µM octyl ester of (R)-2-hydroxyglutarate ((R)-2-HG) or 1-octanol (octyl), and then treated with 1 µM ATRA or vehicle for 24 hrs, again resulting in 4 groups of samples (Octyl-CTRL, Octyl-ATRA, 2HG-CTRL, 2HG-ATRA). All assays were performed in triplicate (4 replicates for Mutant-CTRL and Mutant-ATRA).
2017-03-01 | E-MTAB-4327 | biostudies-arrayexpress
Project description:All-Trans-Retinoic Acid Treatment of IDH Mutant Astrocytes
| PRJNA721930 | ENA
Project description:IDH mutant cells are deficient in retinoic acid production, which impacts downstream gene expression and pathways. We looked at the effect of supplementing IDH mutant glioma cells with ATRA on gene expression and downstream pathways. We compared gene expression changes with IDH WT cells that were also treated with ATRA
2019-12-11 | GSE141789 | GEO
Project description:Ollier disease and Maffucci syndrome are non-hereditary skeletal disorders characterized by multiple enchondromas (Ollier) combined with spindle cell hemangiomas (Maffucci). We found somatic heterozygous IDH1 mutations (R132C and R132H) in 83% of enchondromas, benign cartilage tumors, as well as in 40% of spindle cell hemangiomas, benign vascular lesions. In total, 33 of 42 (78%) patients with Ollier disease and 7 of 13 (54%) patients with Maffucci syndrome carried a mutation in at least one of their tumors. Twelve patients with multiple tumors at different locations displayed identical mutations in separate lesions. Immunohistochemical staining for the R132H IDH1 mutant protein suggested intraneoplastic as well as somatic mosaicism. IDH1 mutations were less frequent (63%) in high grade malignant cartilage tumors in Ollier disease, suggesting that IDH1 is less important for malignant transformation. IDH1 and IDH2 mutations were found in 36% of sporadic cartilage tumors and in four cell lines derived from sporadic chondrosarcomas. 16 samples were analyzed in two color experiment, using normal male or female as a reference sample (gender mismatched)
2011-11-05 | E-GEOD-30354 | biostudies-arrayexpress
Project description:Ollier disease and Maffucci syndrome are non-hereditary skeletal disorders characterized by multiple enchondromas (Ollier) combined with spindle cell hemangiomas (Maffucci). We found somatic heterozygous IDH1 mutations (R132C and R132H) in 83% of enchondromas, benign cartilage tumors, as well as in 40% of spindle cell hemangiomas, benign vascular lesions. In total, 33 of 42 (78%) patients with Ollier disease and 7 of 13 (54%) patients with Maffucci syndrome carried a mutation in at least one of their tumors. Twelve patients with multiple tumors at different locations displayed identical mutations in separate lesions. Immunohistochemical staining for the R132H IDH1 mutant protein suggested intraneoplastic as well as somatic mosaicism. IDH1 mutations were less frequent (63%) in high grade malignant cartilage tumors in Ollier disease, suggesting that IDH1 is less important for malignant transformation. IDH1 and IDH2 mutations were found in 36% of sporadic cartilage tumors and in four cell lines derived from sporadic chondrosarcomas.
2011-11-05 | GSE30354 | GEO
Project description:Expression profile for hemocytes from hml-Gal4, UAS-2xEGFP larvae were compared to hemocytes from hml-Gal4, UAS-2xEGFP; UAS-Idh-R195H larvae We sought to determine which genes and pathways were upregulated or downregulated in hemocytes expressing Idh-R195H, the Drosophila homolog of the human cancer-associated IDH1-R132H mutant, in vivo. We sought to obtain homogeneous populations of hemocytes from each genotype. We compared larvae expressing Idh-R195H from the hml-Gal4 driver to larvae with the hml-Gal4 driver alone.
2014-10-03 | E-GEOD-62008 | biostudies-arrayexpress
Project description:The main purpose of this clinical trial is to learn about the good and the bad effects of all trans retinoic acid (ATRA), atezolizumab and bevacizumab as a possible treatment for advanced colorectal patients.
Participants will be treated with the following combination of these drugs:
1. ATRA will be given in a pill form to be taken twice a day at home for 7 days starting on day 1 of a cycle.
2. Atezolizumab will be given through a vein in arm or through mediport over 60-90 minutes every 2 weeks in the outpatient chemotherapy infusion centers at UTSW.
3. Bevacizumab will be given through a vein in arm or through mediport over 20-40 minutes every 2 weeks in the outpatient chemotherapy infusion centers at UTSW.
| 70824 | ecrin-mdr-crc
Project description:IDH1-R132H is expressed in Low Grade Glioma (LGG) in combination with mutation in ATRX and TP53 genes. IDH1-R132H results in gain of function with production of 2-hydroxygluatrate, that in turn generates a hypermethylatyed phenotype in DNA and histone with consequences in epigenetic regulation of gene expression. Here we will compare the gene expression profile between IDH1-R132H and IDH1 Wt tumor neurospheres.
2019-03-18 | GSE94974 | GEO
Project description:Mutations in the genes encoding isocitrate dehydrogenase 1 and 2 (IDH1/2) occur in a variety of tumor types, resulting in production of the proposed oncometabolite, 2-hydroxyglutarate (2-HG). How mutant IDH and 2-HG alter signaling pathways to promote cancer, though, remains unclear. Additionally, there exist relatively few cell lines with IDH mutations. To examine the effect of endogenous IDH mutations and 2-HG, we created a panel of isogenic epithelial cell lines with either wild-type IDH1/2 or clinically relevant IDH1/2 mutations. Differences were noted in the ability of IDH mutations to cause robust 2-HG accumulation. IDH1/2 mutants that produce high levels of 2-HG cause an epithelial-mesenchymal transition (EMT)-like phenotype, characterized by changes in EMT-related gene expression and cellular morphology. 2-HG is sufficient to recapitulate aspects of this phenotype in the absence of an IDH mutation. In the cells types examined, mutant IDH-induced EMT is dependent on upregulation of the transcription factor ZEB1 and downregulation of the mir-200 family of microRNAs. Furthermore, sustained knockdown of IDH1 in IDH1 R132H mutant cells is sufficient to reverse many characteristics of EMT, demonstrating that continued expression of mutant IDH is required to maintain this phenotype. These results suggest mutant IDH proteins can reversibly deregulate discrete signaling pathways that contribute to tumorigenesis 9 HCT116 isogenic clones with wild-type or IDH1/2 mutations. Samples were analyzed in duplicate.
2012-10-25 | E-GEOD-41802 | biostudies-arrayexpress