GEO DataSets

(Submitter supplied) To investigate the mechanisms by which SYK inhibition sensitizes OCI-mIDH1/N cells to ivosidenib, we performed RNA sequencing (RNA-seq) analysis of cells treated with DMSO (vehicle control), ivosidenib alone, fostamatinib alone, entospletinib alone, or the combination of ivosidenib with each of the two SYK inhibitors for 9 days.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

12 Samples

Download data: CSV

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL24247 GPL17021

18 Samples

Download data

(Submitter supplied) To study the mechanism of resistance to ivosidenib, we developed a model of acquired drug resistance by treating ivosidenib-sensitive OCI-mIDH1/N cells continuously with ivosidenib in culture for a period of 2 months followed by a drug washout period. The resulting cell population (OCI-mIDH1/N-R cells) failed to differentiate upon ivosidenib treatment. We then performed RNA sequencing (RNA-seq) analysis of OCI-mIDH1/N and OCI-mIDH1/N-R cells.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

6 Samples

Download data: CSV

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Methylation profiling by array

Platforms:

GPL20301 GPL21145

156 Samples

Download data: IDAT

(Submitter supplied) Allosteric inhibitors of mutant IDH1 or IDH2 induce terminal differentiation in mutant leukemic blasts and may provide durable clinical responses in approximately 40% of acute myeloid leukemia (AML) patients with the mutations. However, most responders eventually relapse. To understand the molecular underpinnings of clinical resistance, we performed multipronged genomic analyses (DNA sequencing, RNA sequencing and cytosine methylation profiling) in longitudinally collected specimens from 68 IDH1/IDH2-mutant AML patients treated with IDH inhibitors (IDHi), and described the evolution of AML genome and epigenome during the therapy and its association with clinical response and relapse. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

51 Samples

Download data: TXT

(Submitter supplied) Allosteric inhibitors of mutant IDH1 or IDH2 induce terminal differentiation in mutant leukemic blasts and may provide durable clinical responses in approximately 40% of acute myeloid leukemia (AML) patients with the mutations. However, most responders eventually relapse. To understand the molecular underpinnings of clinical resistance, we performed multipronged genomic analyses (DNA sequencing, RNA sequencing and cytosine methylation profiling) in longitudinally collected specimens from 68 IDH1/IDH2-mutant AML patients treated with IDH inhibitors (IDHi), and described the evolution of AML genome and epigenome during the therapy and its association with clinical response and relapse. more...

Organism:

Homo sapiens

Type:

Methylation profiling by array

Platform:

GPL21145

105 Samples

Download data: IDAT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing

Platforms:

GPL19057 GPL24247

32 Samples

Download data: MTX, TSV

(Submitter supplied) Acute myeloid leukemia (AML) tumors are comprised of multiple cell types with distinct capabilities to propagate the disease and resist therapy. Approximately 20% of AML patients carry gain-of-function mutations in isocitrate dehydrogenase (IDH) 1 or -2 that result in over-production of the onco-metabolite D-2-hydroxyglutarate (2-HG). Small molecule inhibitors that block 2-HG synthesis can induce complete morphological remission even in heavily pre-treated AML patients. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

2 Samples

Download data: MTX, TSV

(Submitter supplied) Acute myeloid leukemia (AML) tumors are comprised of multiple cell types with distinct capabilities to propagate the disease and resist therapy. Approximately 20% of AML patients carry gain-of-function mutations in isocitrate dehydrogenase (IDH) 1 or -2 that result in over-production of the onco-metabolite D-2-hydroxyglutarate (2-HG). Small molecule inhibitors that block 2-HG synthesis can induce complete morphological remission even in heavily pre-treated AML patients. more...

Organism:

Mus musculus

Type:

Methylation profiling by high throughput sequencing

Platform:

GPL24247

8 Samples

Download data: TXT

(Submitter supplied) Acute myeloid leukemia (AML) tumors are comprised of multiple cell types with distinct capabilities to propagate the disease and resist therapy. Approximately 20% of AML patients carry gain-of-function mutations in isocitrate dehydrogenase (IDH) 1 or -2 that result in over-production of the onco-metabolite D-2-hydroxyglutarate (2-HG). Small molecule inhibitors that block 2-HG synthesis can induce complete morphological remission even in heavily pre-treated AML patients. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

14 Samples

Download data: TXT, XLSX

(Submitter supplied) Acute myeloid leukemia (AML) tumors are comprised of multiple cell types with distinct capabilities to propagate the disease and resist therapy. Approximately 20% of AML patients carry gain-of-function mutations in isocitrate dehydrogenase (IDH) 1 or -2 that result in over-production of the onco-metabolite D-2-hydroxyglutarate (2-HG). Small molecule inhibitors that block 2-HG synthesis can induce complete morphological remission even in heavily pre-treated AML patients. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

8 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by array; Methylation profiling by high throughput sequencing

Platforms:

GPL13112 GPL6246

22 Samples

Download data: BED, CEL

(Submitter supplied) Mutations in IDH1 and IDH2 are frequently observed in various cancers, including acute myeloid leukemia (AML). Mutant IDHs convert α-ketoglutarate (α-KG) to 2-hydroxyglutarate (2-HG), which dysregulates a set ofα-KG-dependent dioxygenases. To determine whether mutant IDHs are valid targets for cancer therapy, we established a mouse AML model harboring an IDH2 mutation by transplanting mice with nucleophosmin1 (NPM1)+/- mouse hematopoietic stem/progenitor cells that had been co-transduced with four mutant genes (NPMc, IDH2/R140Q, DNMT3A/R882H and FLT3/ITD) that frequently occur simultaneously in human AML patients. more...

Organism:

Mus musculus

Type:

Methylation profiling by high throughput sequencing

Platform:

GPL13112

3 Samples

Download data: BED

(Submitter supplied) Mutations in IDH1 and IDH2 are frequently observed in various cancers, including acute myeloid leukemia (AML). Mutant IDHs convert α-ketoglutarate (α-KG) to 2-hydroxyglutarate (2-HG), which dysregulates a set ofα-KG-dependent dioxygenases. To determine whether mutant IDHs are valid targets for cancer therapy, we established a mouse AML model harboring an IDH2 mutation by transplanting mice with nucleophosmin1 (NPM1)+/- mouse hematopoietic stem/progenitor cells that had been co-transduced with four mutant genes (NPMc, IDH2/R140Q, DNMT3A/R882H and FLT3/ITD) that frequently occur simultaneously in human AML patients. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

19 Samples

Download data: CEL

(Submitter supplied) Mutations in the enzymes IDH1 and IDH2 have been identified in a wide variety of tumors like glioma, chondrosarcoma, thyroid cancer, lymphoma, melanoma, and in acute myeloid leukemia. Mutated IDH1/2 produces the metabolite 2-hydroxyglutarate (2HG), which interferes with epigenetic regulation of gene expression, and thus may promote tumorigenesis.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

9 Samples

Download data: CEL

(Submitter supplied) Mutations in the enzymes IDH1 and IDH2 have been identified in a wide variety of tumors like glioma, chondrosarcoma, thyroid cancer, lymphoma, melanoma, and in acute myeloid leukemia. Mutated IDH1/2 produces the metabolite 2-hydroxyglutarate (2HG), which interferes with epigenetic regulation of gene expression, and thus may promote tumorigenesis.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

6 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array; Methylation profiling by high throughput sequencing

Platforms:

GPL11154 GPL16686

13 Samples

Download data: CEL, CHP, RPT, TXT

(Submitter supplied) Neomorphic mutations in isocitrate dehydrogenase 1 (IDH1) are driver mutations in acute myeloid leukemia (AML) and other cancers. We report the development of new allosteric inhibitors of mutant IDH1. Crystallographic and biochemical results demonstrated that compounds of this chemical series bind to an allosteric site and lock the enzyme in a catalytically inactive conformation, thereby enabling inhibition of different clinically relevant IDH1 mutants. more...

Organism:

Homo sapiens

Type:

Methylation profiling by high throughput sequencing

Platform:

GPL11154

6 Samples

Download data: TXT

(Submitter supplied) Neomorphic mutations in isocitrate dehydrogenase 1 (IDH1) are driver mutations in acute myeloid leukemia (AML) and other cancers. We report the development of new allosteric inhibitors of mutant IDH1. Crystallographic and biochemical results demonstrated that compounds of this chemical series bind to an allosteric site and lock the enzyme in a catalytically inactive conformation, thereby enabling inhibition of different clinically relevant IDH1 mutants. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL16686

7 Samples

Download data: CEL, CHP, RPT

(Submitter supplied) Since characterization of molecular alterations in elderly acute myeloid leukemia (AML) patients using comprehensive studies are lacking, we investigated genetic and epigenetic alterations to unravel the specific background of this unfavorable disease. We studied AML patients by sequencing 555 genes on an Illumina HiSeq2000 platform and investigated DNA methylation profiles using the Illumina 450K array.

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL13534

79 Samples

Download data: TXT