Similar studies for GEO DataSets (Select 200227874) - GEO DataSets

Select item 2002278741.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia [scRNA-seq]

(Submitter supplied) While transcription factor C/AAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPα and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL18573
6 Samples

Download data: TAR

Series

Accession:: GSE227874

ID:: 200227874

PubMed Similar studies

Select item 2002278392.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia [batch1-3]

(Submitter supplied) While transcription factor C/AAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPα and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL18573
39 Samples

Download data: TSV

Series

Accession:: GSE227839

ID:: 200227839

Select item 2002274003.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia [ATAC-seq]

(Submitter supplied) While transcription factor C/AAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPα and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). more...

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL21697
4 Samples

Download data: TSV

Series

Accession:: GSE227400

ID:: 200227400

PubMed Similar studies

Select item 2002264614.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia

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

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL23159
66 Samples

Download data: CEL

Series

Accession:: GSE226461

ID:: 200226461

Select item 2002264605.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia [PDX_GILT_in vivo]

(Submitter supplied) While transcription factor C/AAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPα and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL23159
6 Samples

Download data: CEL, TXT

Series

Accession:: GSE226460

ID:: 200226460

Select item 2002264596.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia [PDX_QUIZ_ex vivo]

(Submitter supplied) While transcription factor C/AAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPα and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL23159
6 Samples

Download data: CEL, TXT

Series

Accession:: GSE226459

ID:: 200226459

Select item 2002264577.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia [MOLM14_shCEBPA+DOX]

(Submitter supplied) While transcription factor C/AAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPα and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL23159
6 Samples

Download data: CEL, TXT

Series

Accession:: GSE226457

ID:: 200226457

Select item 2002264238.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia [MOLM14_shCEBPAconstit]

(Submitter supplied) While transcription factor C/AAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPα and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL23159
6 Samples

Download data: CEL, TXT

Series

Accession:: GSE226423

ID:: 200226423

Select item 2002264229.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia [MOLM14_siCEBPA]

(Submitter supplied) While transcription factor C/AAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPα and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL23159
6 Samples

Download data: CEL, TXT

Series

Accession:: GSE226422

ID:: 200226422

Select item 20022642010.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia [MV411_QUIZ]

(Submitter supplied) While transcription factor C/AAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPα and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL23159
6 Samples

Download data: CEL, TXT

Series

Accession:: GSE226420

ID:: 200226420

Select item 20022641911.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia [MV411_shFLT3]

(Submitter supplied) While transcription factor C/AAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPα and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL23159
6 Samples

Download data: CEL, TXT

Series

Accession:: GSE226419

ID:: 200226419

Select item 20022641812.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia [MOLM14_QUIZ]

(Submitter supplied) While transcription factor C/AAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPα and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL23159
6 Samples

Download data: CEL, TXT

Series

Accession:: GSE226418

ID:: 200226418

Select item 20022641613.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia [MOLM14_shFLT3]

(Submitter supplied) While transcription factor C/AAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPα and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL23159
6 Samples

Download data: CEL, TXT

Series

Accession:: GSE226416

ID:: 200226416

Select item 20022641414.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress-induced ferroptosis in FLT3-mutant leukemia [CEBPAOE_QUIZ]

(Submitter supplied) While transcription factor C/AAT-enhancer binding protein α (C/EBPα) is critical for normal and leukemic differentiation, its role on cell and metabolic homeostasis is largely unknown in cancer. Here, multi-omics analyses uncovered a coordinated activation of C/EBPα and Fms-like tyrosine kinase 3 (FLT3) that increased lipid anabolism in vivo and in patients with FLT3-mutant acute myeloid leukemia (AML). more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL23159
12 Samples

Download data: CEL, TXT

Series

Accession:: GSE226414

ID:: 200226414

Select item 20014475915.

Synergistic Targeting of FLT3 Mutations in AML via Combined Menin-MLL and FLT3 Inhibition

(Submitter supplied) The interaction of Menin (MEN1) and MLL (MLL1, KMT2A) is a dependency and potential therapeutic opportunity against NPM1 mutant (NPM1mut) and MLL-rearranged (MLL-r) leukemias. Concomitant activating driver mutations in the gene encoding the tyrosine kinase FLT3 occur in both leukemias and are particularly common in the NPM1mut subtype. Transcriptional profiling upon pharmacological inhibition of the Menin-MLL complex revealed specific changes in gene expression with downregulation of the MEIS1 transcription factor and its transcriptional target gene FLT3 being most pronounced. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL20301
24 Samples

Download data: TXT

Series

Accession:: GSE144759

ID:: 200144759

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 20010516116.

Glutaminolysis is a metabolic dependency in FLT3 ITD Acute Myeloid Leukemia unmasked by FLT3 Tyrosine Kinase Inhibition

(Submitter supplied) FLT3ITD are common mutations in Acute Myeloid Leukemia (AML) and carry a particularly bad prognosis. Although new generation FLT3 tyrosine kinase inhibitors (TKI) have shown promising results, the outcome of FLT3-mutated AML patients remains poor and demands the identification of novel, specific and validated therapeutic targets for this highly aggressive AML subtype. Utilizing an unbiased genome-wide CRISPR/Cas9 screen, we identify GLS, the first enzyme in glutamine metabolism, as synthetically lethal with FLT3 TKI treatment. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL20301
12 Samples

Download data: BW

Series

Accession:: GSE105161

ID:: 200105161

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 20013392517.

CircMYBL2 Regulates FLT3-ITD FLT3AML Translation in AML

(Submitter supplied) CircMYBL2 is more highly expressed in AML patients with FLT3-ITD mutations than in those without the FLT3-ITD mutation. We found that circMYBL2 knockdown specifically inhibits proliferation and promotes the differentiation of FLT3-ITD AML cells in vitro and in vivo. We used the ribosome profiling and RNA-seq libraries sequenced with Illumina HiSeq 2500 to identify the mRNA that circMYBL2 targeted. Interestingly, we found that circMYBL2 significantly influences the protein level of mutant FLT3 kinase, which contributes to the activation of FLT3-ITD-dependent signaling pathways. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing; Other

Platform:: GPL24676
8 Samples

Download data: CSV, TXT

Series

Accession:: GSE133925

ID:: 200133925

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 20016393218.

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia

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

Organism:: Homo sapiens; Mus musculus

Type:: Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platforms:: GPL19057 GPL18573
37 Samples

Download data: BW, NARROWPEAK

Series

Accession:: GSE163932

ID:: 200163932

PubMed Similar studies

Select item 20016393019.

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_DMSO_AC220_24hr]

(Submitter supplied) We performed 3'-RNA-Sequencing on RNA isolated from human MV4-11 and OCI-AML3 cells which had been treated with DMSO or the FLT3 inhibitor Quizartinib (AC220) to perform differential gene expression analysis.

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL18573
12 Samples

Download data: CSV

Series

Accession:: GSE163930

ID:: 200163930

Select item 20016392720.

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VIVO]

(Submitter supplied) We performed 3'-RNA-Sequencing on RNA isolated from murine MLL-AF9/iFLT3-ITD cells where the inducible iFLT3-ITD transgene had been depleted for 48 hours compared to non-depleted conditions in vivo to perform differential gene expression analysis.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL19057
6 Samples

Download data: CSV

Series

Accession:: GSE163927

ID:: 200163927

PubMed Similar studies SRA Run Selector

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