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Identification of transcriptional network regulated by FGFR1 fusion kinase in stem cell leukemia and lymphoma (SCLL)

ABSTRACT: Identification of transcriptional network regulated by FGFR1 fusion kinase in stem cell leukemia and lymphoma (SCLL)

PROVIDER: PRJNA433808 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6706340_1.fastq.gz	Fastqsanger.gz
	SRR6706340_2.fastq.gz	Fastqsanger.gz
	SRR6706341_1.fastq.gz	Fastqsanger.gz
	SRR6706341_2.fastq.gz	Fastqsanger.gz
	SRR6706342_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Identification of transcriptional network regulated by FGFR1 fusion kinase in stem cell leukemia and lymphoma (SCLL)

Project description:Purpose: Oncogenic transformation of hematopoietic stem cells by chimeric fusion kinases causing constitutive activation of FGFR1 leads to a stem cell leukemia/lymphoma (SCLL) syndrome, accompanied by widespread dysregulation of gene activity. The goals of this study are to use NGS-derived transcriptome profiling (RNA-seq) to identify genes regulated by FGFR1 fusion kinase in SCLL. Methods: Three different cell models for SCLL, respectively BBC2 (B cell lymphoblastic leukemia/lymphoma), ZNF112 (B cell lymphoblastic leukemia/lymphoma) and BCRF8C (myloid leukemia) were treated with selective FGFR1 kinase inhibitor,then the total RNA from treatment and viechel control were isolated for RNA-Seq analysis. Results: A global gene experssion change is generated, and provides fundamental information for demostration of molecular mechanisms in FGFR1 driven leukemogenesis.

2019-02-12 | GSE110457 | GEO

ZMYM2/FGFR1, BCR/FGFR1 or BCR/ABL1 in human cord blood CD34+ cells reveals similar but distinct gene expression profiles

Project description:The 8p11 myeloproliferative syndrome (EMS), also referred to as the stem cell leukemia/lymphoma syndrome, is a chronic myeloproliferative disorder that rapidly progresses into an acute leukemia. Molecularly, EMS is characterized by fusion of various partner genes to the FGFR1 gene, resulting in constitutive activation of the tyrosine kinase activity within FGFR1. The two most common fusion genes in human EMS are ZMYM2/FGFR1 (previously known as ZNF198/FGFR1) and BCR/FGFR1. To study the transcriptional programs becoming deregulated by the FGFR1 fusion genes, global gene expression analysis on human CD34+ cord blood cells expressing either of the fusion oncogenes ZMYM2/FGFR1 and BCR/FGFR1 was performed. As a reference gene we also included the more studied BCR/ABL1 fusion oncogene associated with chronic myeloid leukemia. We found that the 3 different fusion oncogenes had in common the upregulation of several genes involved in the JAK/STAT signalling pathway and also other sets of genes. However, the gene expression profiles were not identical, suggesting that both the tyrosine kinase containing gene and the partner gene would affect the transcription of downstream target genes. Bicistronic retroviral murine stem cell virus (MSCV) vectors expressing ZMYM2/FGFR1, BCR/FGFR1or P210 BCR/ABL1 and GFP were used. The MIG control vector expressed GFP only. Two days post transfection of human CD34+ umbilical cord blood cells, GFP-sorted cells were collected in three biological replicates and RNA was isolated immediately. In total, 12 samples were hybridized and scanned.

2010-05-27 | E-GEOD-15811 | biostudies-arrayexpress

ZMYM2/FGFR1, BCR/FGFR1 or BCR/ABL1 in human cord blood CD34+ cells reveals similar but distinct gene expression profiles

2010-05-01 | GSE15811 | GEO

Genome-wide profiling of miRNA associated with BCR-FGFR1 fusion kinase driven stem cell leukemia and lymphoma II

Project description:The BBC1 and BBC2 cell lines were isolated from pre-B-cell lymphoma models of a murine BCR-FGFR1 driven SCLL. miRNA profiles for BBC2 cells, were established using miRNA arrays. First, BBC2 cells were compared with FACS sorted, normal, murine splenic CD19+ B cells isolated from BALB/c mice, where upregulated and downregulated miRNAs in BBC2 cells were identified. We next investigated which of these miRNAs were affected by loss of FGFR1 function. Previously we showed that the FGFR inhibitor BGJ398 suppresses suppressed phosphoactivation of chimeric FGFR1 kinases. When BBC2 cells were treated with 50nM BGJ398 for 24 hours, up- and down-regulated miRNAs by FGFR1 signaling were identified. By comparasion of the two subsets of differentially expressed miRNAs, we were able to define core candidate miRNAs which appear to be regulated by BCR-FGFR1 in SCLL.

2018-01-01 | GSE104895 | GEO

Genome-wide profiling of miRNA associated with BCR-FGFR1 fusion kinase driven stem cell leukemia and lymphoma I

2018-01-01 | GSE104894 | GEO

Genome-wide profiling of miRNA associated with BCR-FGFR1 fusion kinase driven stem cell leukemia and lymphoma II

Project description:Genome-wide profiling of miRNA associated with BCR-FGFR1 fusion kinase driven stem cell leukemia and lymphoma II

| PRJNA414101 | ENA

Genome-wide profiling of miRNA associated with BCR-FGFR1 fusion kinase driven stem cell leukemia and lymphoma I

Project description:Genome-wide profiling of miRNA associated with BCR-FGFR1 fusion kinase driven stem cell leukemia and lymphoma I

| PRJNA414102 | ENA

Gene expression profile of Baf3 cells overexpressing TPR-FGFR1 fusion gene

Project description:Nowadays, fibroblast growth factor receptor 1 (FGFR1) inhibitors are considered as an effective kinase inhibitor for 8p11 myeloproliferative syndrome (EMS) treatment. However, targeting FGFR1 alone may not be sufficient in EMS patients with TPR-FGFR1 rearrangement. In this study, we established TPR FGFR1 expressing Baf3 cells and performed RNA-Seq analysis. RNA-Seq analysis revealed that genes associated with TPR-FGFR1 expression mainly participated in the epidermal growth factor receptor (EGFR) pathway (|FC| > 1.80, P < 0.05). Gene set enrichment analysis (GSEA) identified significant enrichment in the PI3K/AKT pathways. We found that EGFR is another activation pathway for AKT in TPR-FGFR1-expressing Baf3 cells. Moreover, we found that treatment with FGFR1 inhibitors alone could completely inhibit FGFR1 phosphorylation, but could not completely inhibit AKT, which is the downstream molecule of FGFR1. Compared to FGFR1 inhibitors alone, co-treatment with PD-166866 (FGFR1 inhibitor) and MK-2206 (AKT inhibitor) could simultaneously inhibit the phosphorylation of FGFR1 and AKT. In addition, FACS results indicated that the combination therapy of PD-168866 and MK-2206 significantly increased the rate of cells apoptosis than monotherapy of PD-166866 (P < 0.0001). Collectively, the data obtained in the present study provides strong evidence for dual targeting therapy of FGFR1 and AKT in EMS patients with TPR-FGFR1 rearrangement, offering a new direction for EMS treatment.

2024-07-21 | GSE272597 | GEO

Expression data from ZMYM2-FGFR1-induced T-cell lymphomas in a mouse model

Project description:The ZMYM2-FGFR1 (formerly known as ZNF198-FGFR1) fusion kinase induces stem cell leukemia-lymphoma syndrome (SCLL), a hematological malignancy characterized by rapid transformation to acute myeloid leukemia and T-lymphoblastic lymphoma. We previously developed a mouse model of ZMYM2-FGFR1 (Ren et al. 2009, Blood). To further investigate mechanisms of oncogenesis and progression, we undertook a global gene expression analysis of leukemic T-cells from the animal model compared with Thy1+DP+ (CD4+CD8+) cells isolated from normal Balb/c thymuses, as well as lukemic stem cells (LSK, GFP+Lin-Sca-1+c-kit+ cells) sorted from the leukemic mice versus hematopoietic stem cells (HSC, Lin-Sca-1+c-kit+ cells) sorted from normal BALB/c bone marrow cells. We found high expressions of Notch1 and its downstream target genes in T-cell lymphomas that arise in a murine model of ZMYM2-FGFR1 SCLL. Our functional studies demonstrate the importance of Notch signaling in the etiology of SCLL and suggest that targeting this pathway could provide a novel strategy for molecular therapies to treat SCLL patients.

2012-02-14 | GSE28823 | GEO

Epigenome analysis of low-grade neuroepithelial tumors with FGFR1 alterations

Project description:Genome-wide DNA methylation profiling of 30 low-grade neuroepithelial tumors with FGFR1 alterations including rosette-forming glioneuronal tumor, pilocytic astrocytoma, dysembryoplastic neuroepithelial tumor, and extraventricular neurocytoma. The Illumina Infinium EPIC 850k Human DNA Methylation Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpG sites of genomic DNA extracted from formalin-fixed, paraffin-embedded tumor tissue of 30 low-grade neuroepithelial tumors with FGFR1 alterations including kinase domain tandem duplication, in-frame fusion with TACC1, and hotspot missense mutation within the intracellular tyrosine kinase domain.

2020-08-19 | GSE152653 | GEO

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