Expression studies of FGFR1 knockdown in lymphoma
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ABSTRACT:
PROVIDER: PRJNA929205 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression signatures for FGFR1 Knockdown in Mantle cell lymphoma cell line (Z-138)
| PRJNA574838 | ENA
Project description:To identify the differential regulated genes among cell types
2025-02-02 | GSE223954 | GEO
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
Project description:To understand the role of FGFR1 in the MCL progression.
2020-05-01 | GSE138127 | GEO
Project description:Human glioblastoma cell lines L0, L1, L2 (Deleyrolle et al. Brain 2010) were transduced with lentivirus vectors expressing scrambled control (shCo), FGFR1 knockdown (shFGFR1), or FGFR2 knockdown (shFGFR2) sequences. Cells were cultured in N2 medium containing EGF and stimulated with FGF2 for 48 hours prior to RNA extraction.
2023-08-29 | E-MTAB-13161 | biostudies-arrayexpress
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
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
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.
2010-05-01 | GSE15811 | GEO
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
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 | GSE104894 | GEO