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Links from GEO DataSets

Items: 20

1.

Gene expression analysis of parental cell lines and cell lines with acquired resistance to compound 3 (C03) and compound 7 (C07).

(Submitter supplied) Cells were cultured for a period of six months in slowly escalating concentrations of two small molecules (Compound 3 and Compund 7) whose protein target was unknown. Over this six month period, the cells cultured in C03 and C07 became resistant to the differentiation and growth inhibitory effects of the the compounds. Total RNA was harvested for RNA-sequencing.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL13112 GPL11154
6 Samples
Download data: TXT
Series
Accession:
GSE84875
ID:
200084875
2.

Time course of myeloid differentiation in the Lysozyme-GFP ER-HoxA9 cells following estradiol withdrawal

(Submitter supplied) Lysozyme-GFP ER-HoxA9 cells were cultured in the presence of estradiol (active ER-HoxA9) or in the absence of estradiol (inactive ER-HoxA9). Samples were taken at 10 time points over a 120 hour time course of myeloid differentiation to examine those gene expression changes that accompany differentiation upon the release of HoxA9 differentiation arrest.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
24 Samples
Download data: TXT
Series
Accession:
GSE84874
ID:
200084874
3.

Gene expression of MLL/AF9 leukemia cells sorted from mice treated with or without brequinar

(Submitter supplied) Mice bearing an MLL/AF9 leukemia were treated with vehicle or brequinar every three days for a total of four doses. Mice were euthanized for collection of the bone marrow cells. The leukemia cells were purified by FACS (fluorescence activated cell sorting) and total RNA was prepared from the purified leukemia cells.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
2 Samples
Download data: TXT
Series
Accession:
GSE84873
ID:
200084873
4.

Inhibition of pyrimidine biosynthesis targets protein translation in AML

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other
Platform:
GPL19057
43 Samples
Download data
Series
Accession:
GSE181666
ID:
200181666
5.

Inhibition of pyrimidine biosynthesis targets protein translation in AML [Targeted_CRISPR_screen]

(Submitter supplied) Investigating genes that increase or decrease treatment efficacy of AG636 in MLL-AF9; KrasG12D (MN) AML cells.
Organism:
Mus musculus
Type:
Other
Platform:
GPL19057
7 Samples
Download data: TXT
Series
Accession:
GSE181665
ID:
200181665
6.

Inhibition of pyrimidine biosynthesis targets protein translation in AML [RNA-seq_RUNX1]

(Submitter supplied) Investigation of the transcriptional profile of AML in response to DHODH inhibition by AG636. RUNX1-RUNX1T1 cells were transplanted into Ptprca recipients. Mice bearing tumors were treated with AG636 for one day. Leukemic stem cells (cKit high; CD11b low) from bone marrow and spleen were isolated and RNA sequencing performed.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: TXT
Series
Accession:
GSE181664
ID:
200181664
7.

Inhibition of pyrimidine biosynthesis targets protein translation in AML [RNA-seq_I1DN]

(Submitter supplied) Investigation of the transcriptional profile of AML in response to DHODH inhibition by AG636. I1DN model was generated by co-transduction of foetal liver derived HSPCs with constructs encoding IDH1R132H, DNMT3AR882H and NrasG12D. Cells were transplanted into Ptprca recipients. Mice bearing I1DN tumors were treated with AG636 for one day. Leukemic stem cells (cKit high; CD11b low) from bone marrow and spleen were isolated and RNA sequencing performed.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: TXT
Series
Accession:
GSE181663
ID:
200181663
8.

Inhibition of pyrimidine biosynthesis targets protein translation in AML [RNA-seq_MN-2]

(Submitter supplied) Investigation of the transcriptional profile and compared with the genome accessibility (using ATAC-seq) in MN cells. Mice bearing MN tumors were treated with AG636 for 2 days. Leukemic stem cells (cKit high; CD11b low) from bone marrow and spleen were isolated. RNA sequencing and ATAC-seq were performed.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
4 Samples
Download data: TXT
Series
Accession:
GSE181662
ID:
200181662
9.

Inhibition of pyrimidine biosynthesis targets protein translation in AML [RNA-seq_MN]

(Submitter supplied) Investigation of the transcriptional profile of MLL-rearranged AML in response to DHODH inhibition by AG636. Chemo-refractory syngeneic murine AML model driven by doxycycline-inducible expression of MLL-AF9 and constitutive expression of oncogenic Nras (MN) was transplanted into Ptprca recipients. Mice bearing MN tumors were treated with doxycycline or AG636 for one or four days. Leukemic stem cells (cKit high; CD11b low) from bone marrow and spleen were isolated and RNA sequencing performed.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
14 Samples
Download data: TXT
Series
Accession:
GSE181661
ID:
200181661
10.

Inhibition of pyrimidine biosynthesis targets protein translation in AML [ATAC-seq_MN-2]

(Submitter supplied) Investigation of the chromatin accessibility in MN cells. Mice bearing MN tumors were treated with AG636 for 2 days. Leukemic stem cells (cKit high; CD11b low) from bone marrow and spleen were isolated. RNA sequencing and ATAC-seq were performed.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
4 Samples
Download data: BW
Series
Accession:
GSE181660
ID:
200181660
11.

RNA-seq analysis of AML cells in response to ASLAN003

(Submitter supplied) We aim to gain insight into the changes of gene expression induced by ASLAN003, a novel, potent Dihydroorotate Dehydrogenase (DHODH) Inhibitor
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
12 Samples
Download data: TXT
12.

Hoxa9/meis1-transgenic zebrafish develops acute myeloid leukemia-like disease with rapid onset and high-penetrance

(Submitter supplied) HOXA9/MEIS1 plays a synergistic causative role and overexpresses frequently in acute myeloid leukemia (AML). Hoxa9/Meis1 transgenic murine results in rapid leukemic transformation of primary bone marrow cells. However, murine model is not suitable to perform a high-throughput phenotypic screen in vivo and identify compounds for AML therapy. A transgenic zebrafish overexpresses hoxa9/meis1 need to generate. more...
Organism:
Danio rerio
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24995
6 Samples
Download data: XLSX
Series
Accession:
GSE204744
ID:
200204744
13.

Inhibition of dihydroorotate dehydrogenase by doxorubicin and brequinar sensitize cancer cells to TRAIL-induced apoptosis

(Submitter supplied) Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising agent in selectively killing tumor cells. However, TRAIL monotherapy has not been successful as many cancer cells are resistant to TRAIL. Chemotherapeutic agents, such as doxorubicin have been shown to act synergistically with TRAIL, but the exact mechanisms of actions are poorly understood. In this study, we performed high-throughput small interfering RNA screening and genome-wide gene expression profiling on doxorubicin-treated U1690 cells to explore novel mechanisms underlying doxorubicin-TRAIL synergy. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
8 Samples
Download data: TXT
Series
Accession:
GSE42531
ID:
200042531
14.

The role of Hoxa9 and Meis1 in development of acute myeloid leukemia (mRNA)

(Submitter supplied) OBJECTIVE: MEIS1, a HOX cofactor, collaborates with multiple HOX proteins, such as HOXA9, to accelerate the onset of acute myeloid leukemia (AML) through largely unknown molecular mechanisms. To further resolve these mechanisms, we conducted a structure-function analysis of Meis1 and gene expression profiling, in the context of Hoxa9 leukemogenesis. RESULTS: We show, in a murine bone marrow transplantation model, that the homeodomain of Meis1 is required for leukemogenic collaboration with Hoxa9. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6193
12 Samples
Download data: CEL, CHP
Series
Accession:
GSE75272
ID:
200075272
15.

Elevated acid ceramidase promotes acute myeloid leukemia blast survival through sphingolipid dysregulation and Mcl-1 upregulation

(Submitter supplied) Gene expression of patient samples with acute myeloid leukemia (AML) were compared to normal controls to study dysregulated signalling pathways. Peripheral blood mononuclear cells (PBMCs) from primary AML patient samples were isolated using the Ficoll-Paque gradient separation method. RNA from CD34+ bone marrow cells of healthy donors were purchased from AllCells LLC (Alameda, CA; catalog number RNA-BM003C). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6947
38 Samples
Download data: TXT
Series
Accession:
GSE65409
ID:
200065409
16.

Targeting of Hematologic Malignancies with PTC299, A Novel Potent Inhibitor of Dihydroorotate Dehydrogenase with Favorable Pharmaceutical Properties

(Submitter supplied) PTC299 was identified as an inhibitor of VEGFA mRNA translation in a phenotypic screen and evaluated in the clinic for treatment of solid tumors. To guide precision cancer treatment, we performed extensive biological characterization of the activity of PTC299 and demonstrated that inhibition of VEGF production and cell proliferation by PTC299 is linked to a decrease in uridine nucleotides by targeting dihydroorotate dehydrogenase (DHODH), a rate limiting enzyme for de novo pyrimidine nucleotide synthesis. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
8 Samples
Download data: CEL
Series
Accession:
GSE121266
ID:
200121266
17.

Novel IDH1 Mutant Inhibitors for Treatment of Acute Myeloid Leukemia

(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
Series
Accession:
GSE72253
ID:
200072253
18.

Novel IDH1 Mutant Inhibitors for Treatment of Acute Myeloid Leukemia (ERRBS)

(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
Series
Accession:
GSE72247
ID:
200072247
19.

Novel IDH1 Mutant Inhibitors for Treatment of Acute Myeloid Leukemia (expression)

(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
Series
Accession:
GSE72152
ID:
200072152
20.

Functional diversity of inhibitors tackling the differentiation arrest of MLL-rearranged leukemia

(Submitter supplied) Purpose: The chromosomal rearrangements of the mixed-lineage leukemia (MLL) gene have been extensively characterized as a potent oncogenic driver on the molecular and mechanistic level in acute lymphoblastic (ALL) and acute myeloid (AML) leukemia. For its oncogenic function the MLL fusion protein is hijacking the the multi enzyme super elongation complex (SEC) leading to elevated expression of MLL target genes (e.g. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
305 Samples
Download data: TSV
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