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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression analysis of 12 B-cell Chronic Lymphocytic Leukemia samples and 5 CD19+ control samples

ABSTRACT: Elevated levels of microRNA miR-155 represent a candidate pathogenic factor in chronic B-lymphocytic leukemia (B-CLL). In this study, we present evidence that MYB (v-myb myeloblastosis viral oncogene homolog) is overexpressed in a subset of B-CLL patients. MYB physically associates with the promoter of MIR155 host gene (MIR155HG, also known as BIC, B-cell integration cluster) and stimulates its transcription. This coincides with the hypermethylated histone H3K4 residue and spread hyperacetylation of H3K9 at MIR155HG promoter. Our data provide evidence of oncogenic activities of MYB in B-CLL that include its stimulatory role in MIR155HG transcription. We have studied differentially expressed genes in the whole genome and also in the preselected groups of MYB target genes and miR-155 microRNA predicted targets. This study was intended to investigate differentially expressed genes mRNA in 12 B-CLL patient peripheral blood samples in comparison with 5 CD19+ healthy donor peripheral blood samples.

ORGANISM(S): Homo sapiens

SUBMITTER: Vojtěch Kulvait

PROVIDER: E-GEOD-26725 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression analysis of 12 B-cell Chronic Lymphocytic Leukemia samples and 5 CD19+ control samples

Project description:Elevated levels of microRNA miR-155 represent a candidate pathogenic factor in chronic B-lymphocytic leukemia (B-CLL). In this study, we present evidence that MYB (v-myb myeloblastosis viral oncogene homolog) is overexpressed in a subset of B-CLL patients. MYB physically associates with the promoter of MIR155 host gene (MIR155HG, also known as BIC, B-cell integration cluster) and stimulates its transcription. This coincides with the hypermethylated histone H3K4 residue and spread hyperacetylation of H3K9 at MIR155HG promoter. Our data provide evidence of oncogenic activities of MYB in B-CLL that include its stimulatory role in MIR155HG transcription. We have studied differentially expressed genes in the whole genome and also in the preselected groups of MYB target genes and miR-155 microRNA predicted targets.

2011-03-01 | GSE26725 | GEO

Gene expression data from chronic lymphocytic leukemia samples

Project description:MicroRNA-155 is frequently over-expressed in CLL and is associated with worse clinical prognosis. To understand the role of miR-155 in CLL pathogenesis, we used microarrays to identify genes that are expressed at significantly lower levels in CLLs that harbor higher levels of miR-155 expression in an attempt to determine the relevant gene targets of miR-155 in CLL. MiR-155 levels of 38 CLL samples were determined and ranked. 6 CLLs with the highest and 6 CLLs with the lowest miR-155 within the IgVH unmutated group, and 5 CLLs with the highest and 5 CLLs with the lowest miR-155 within the IgVH mutated group were selected for Affymetrix array analyses.

2011-06-01 | E-GEOD-29605 | biostudies-arrayexpress

Gene expression data from chronic lymphocytic leukemia samples

2011-06-01 | GSE29605 | GEO

Transcription profiling of human chronic lymphocytic leukemia cells treated with valproic acid

Project description:Epigenetic code modifications by histone deacetylase inhibitors (HDACi) have recently been proposed as potential new therapies for hematological malignancies. Chronic Lymphocytic Leukemia (CLL) remains incurable despite the introduction of new treatments. CLL cells are characterized by an apoptosis defect rather than excessive proliferation, but proliferation centers have been found in organs such as bone marrow and lymph nodes. Here, we investigated gene expression modifications in CLL cells following treatment with valproic acid (VPA), a well-tolerated anti-epileptic drug with HDAC inhibitory activity. Experiment Overall Design: CLL cells obtained from 14 patients were treated in vitro with a concentration of 1mM VPA for 4 hours. VPA effects on gene expression were thereafter studied using Affymetrix technology

2009-09-17 | E-GEOD-14973 | biostudies-arrayexpress

MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter

Project description:Most E2F-binding sites repress transcription through the recruitment of Retinoblasoma (RB) family members until the end of the G1 cell-cycle phase. Although the MYB promoter contains an E2F-binding site, its transcription is activated shortly after the exit from quiescence, before RB family members inactivation, by unknown mechanisms. We had previously uncovered a nuclear factor distinct from E2F, Myb-sp, whose DNA-binding site overlapped the E2F element and had hypothesized that this factor might overcome the transcriptional repression of MYB by E2F-RB family members. We have purified Myb-sp and discovered that Myc-associated zinc finger proteins (MAZ) are major components. We show that various MAZ isoforms are present in Myb-sp and activate transcription via the MYB-E2F element. Moreover, while forced RB or p130 expression repressed the activity of a luciferase reporter driven by the MYB-E2F element, co-expression of MAZ proteins not only reverted repression, but also activated transcription. Finally, we show that MAZ binds the MYB promoter in vivo, that its binding site is critical for MYB transactivation, and that MAZ knockdown inhibits MYB expression during the exit from quiescence. Together, these data indicate that MAZ is essential to bypass MYB promoter repression by RB family members and to induce MYB expression.

2017-10-04 | PXD006857 | Pride

Acquired genomic copy number aberrations and survival in chronic lymphocytic leukemia

Project description:Genomic aberrations are of predominant importance to the biology and clinical outcome of patients with chronic lymphocytic leukemia (CLL), and FISH-based genomic risk classifications are routinely used in clinical decision making in CLL. One of the known limitations of CLL FISH is the inability to comprehensively interrogate the CLL genome for genomic changes. In an effort at overcoming the existing limitations in CLL genome analysis, we have analyzed high-purity DNA isolated from FACS-sorted CD19+ cells and paired CD3+ or buccal cells from 255 CLL patients for acquired genomic copy number aberrations (aCNA) using ultra-high-density Affymetrix SNP 6.0 arrays. Overall, two or more subchromosomal aCNA were found in 39% (100/255) of all cases analyzed, while ≥3 subchromosomal aCNA were detected in 20% (50/255) of cases. Subsequently, we have correlated genomic lesion loads (genomic complexity) with the clinical outcome measures time to first therapy (TTFT) and overall survival (OS). Using multivariate analyses incorporating the most important prognostic factors in CLL together with SNP 6.0 array-based genomic lesion loads at various thresholds, we identify elevated CLL genomic complexity as an independent and powerful marker for the identification of CLL patients with aggressive disease and short survival. we have analyzed high-purity DNA isolated from FACS-sorted CD19+ cells and paired CD3+ or buccal cells from 255 CLL patients for acquired genomic copy number aberrations (aCNA) using ultra-high-density Affymetrix SNP 6.0 arrays

2011-11-29 | E-GEOD-30777 | biostudies-arrayexpress

Transcription profiling of human chronic lymphocytic leukemia patients expressing high or low levels of ZAP70 mRNA

Project description:Comparison of Chronic Lymphocytic Leukemia patients expressing high or low levels of ZAP70 mRNA: prognostic factors and interaction with the microenvironment. Zeta-associated protein 70 (ZAP70) is a widely recognized prognostic factor in chronic lymphocytic leukemia (CLL), but mechanisms by which its higher expression leads to a poor outcome remain to be fully explained. In an attempt to unveil unfavorable cellular properties linked to high ZAP70 expression, we used gene expression profiling to identify genes associated with disparities in B-cells from CLL patients expressing high versus low ZAP70 mRNA, measured by quantitative real-time PCR. Experiment Overall Design: Two groups of seven CLL patients were compared, selected on the basis of either high or low ZAP70 mRNA expression. Total RNA from CD19+ purified cells was exctracted and hybidyzed on Affymetrix GeneChipÃÂ® Human Genome U133 Plus 2.0 Array. Amplification, hybridization and scanning were done according to standard Affymetrix protocols (www.affymetrix.com). CEL files were ,normalized with RMA method.

2009-04-25 | E-GEOD-12734 | biostudies-arrayexpress

Clonal evolution, genomic drivers, and effects of therapy in chronic lymphocytic leukemia

Project description:The identification of gene mutation and structural genomic aberrations that are critically involved in CLL pathogenesis is still evolving. One may postulate that genomic driver lesions with effects on CLL proliferation, apoptosis thresholds, or chemotherapy resistance should increase in frequency over time when measured sequentially in a large CLL cohort. We sequentially sampled a large, well-characterized CLL cohort at a mean of 4 years between samplings. The paired analysis included 156 patients, of whom 114 remained untreated and 42 received intercurrent therapies. Results: we identify a strong effect of intercurrent therapies on the frequency of acquisition of aCNAs in CLL. Importantly, the spectrum of acquired genomic changes was largely similar in patients that did or did not receive intercurrent therapies; therefore, various genomic changes that become part of the dominant clones are often already present in CLL cell populations prior to therapy. Further, we provide evidence that therapy of CLL with preexisting TP53 mutations results in the outgrowth of genomically very complex clones which dominate at relapse. Using complementary technologies directed at the detection of genomic events that are present in substantial proportions of of the clinically relevant CLL disease bulk, we capture aspects of genomic evolution in CLL over time, including increases in the frequency of genomic complexity, specific recurrent aCNAs, and TP53 mutations. Data from 156 paired samples (enrollment and one longitudinal sample) are included in this data set. Of these, 27 patients were assayed at two (or, rarely, more than two) time points. Please note: normal DNA and enrollment date tumor DNA CEL files and SNP call files will be found in a separate GEO data submission: GSE30777

2013-04-19 | E-GEOD-45565 | biostudies-arrayexpress

GEP data from BCWM.1 cells treated with LNA antimiR-155 or scramble control

Project description:microRNA-155 acts as an oncogenic miRNA in B-cell lymphoproliferative disorders including Waldenstrom Macroglobulinemia (WM) and Chronic Lymphocytic Leukemia (CLL). we used an 8-mer LNA (locked nucleic acid) phosphorothioate oligonucleotide targeting the seed region of miR-155 to effectively antagonize in vitro tumor growth in WM.

2012-07-10 | GSE39189 | GEO

NK cell array from B-CLL patients

Project description:Chronic lymphocytic leukemia (B-CLL) and small lymphocytic lymphoma (SLL) are part of the same disease classification but are defined by differential distribution of tumor cells. B-CLL is characterized by significant immune suppression and dysregulation but this is nottypical of patients with SLL. Natural killer cells (NK) are important mediators of immune function but have been relatively poorly studied in patients with B-CLL/SLL.

2016-09-30 | E-MTAB-4403 | biostudies-arrayexpress

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