2020_CES_WGBS - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001005970 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:ChIPseq data for 31 CLL samples (12 controls, 19 tumor) of the CancerEpiSys-PRECiSe project; containing histone H3, histone modifications and transcription factor binding sites (CTCF, EBF1).
| EGAD00001005969 | EGA
Project description:Tagged-WGBS for 3 Naive B Cell samples of the CancerEpiSys-PRECiSe project.
| EGAD00001005966 | EGA
Project description:Single-cell ATAC-seq data for 5 CLL samples (2 controls, 3 tumor) of the CancerEpiSys-PRECiSe project.
| EGAD00001005965 | EGA
Project description:ATAC-seq data for 26 CLL samples (7 controls, 19 tumor) of the CancerEpiSys-PRECiSe project.
| EGAD00001005967 | EGA
Project description:long RNA data for 27 CLL samples (8 controls, 19 tumor) of the CancerEpiSys-PRECiSe project.
| EGAD00001005968 | EGA
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. 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.
2011-03-01 | E-GEOD-26725 | biostudies-arrayexpress
Project description:Epidemiological data show that the immune system may control or promote emergence and growth of a neoplastic lymphomatous clone. Conversely, systemic lymphomas, especially myeloma and CLL, are associated with clinical immunodeficiency. This prospective controlled study demonstrates substantially reduced circulating T helper cells, predominantly naive CD4+ cells, in patients with non-leukemic follicular and extranodal marginal zone lymphomas, but not in monoclonal gammopathy and early CLL. These numerical changes were correlated with a preactivated phenotype, hyperreactivity in vitro, presenescence, and a Th2 shift of peripheral T helper cells. No prominent alterations were found in the regulatory T cell compartment. Gene expression profiling of in vitro-stimulated CD4+ cells revealed an independent second alteration of T helper cell physiology which was most pronounced in early CLL but also detectable in FL/eMZL. This pattern consisted of downregulation of proximal and intermediate T-cell receptor signaling cascades and globally reduced cytokine secretion. Both types of T cell dysfunction may contribute to significant immunodeficiency in non-leukemic indolent B-cell lymphomas as demonstrated by refractoriness to hepatitis B vaccination. The precise definition of systemic T cell dysfunction serves as the basis to study its prognostic impact, its relationship to the established influence of the lymphoma microenvironment, and its therapeutic manipulation 8 samples from FL/eMZL patients, 7 samples from CLL patients, 5 samples of MGUS patients, 5 MALT, 16 healthy controls
2011-03-01 | E-GEOD-23293 | biostudies-arrayexpress
Project description:Genome-wide profiling of DNA methylation 35 kb upstream and 5 kb downstream of microRNAs in 24 CLL patients and B cells of 2 healthy donors versus a pool of 10 healthy donors. 26 samples total (24 CLL B cell samples and 2 healthy donor B cell samples) were hybridized against a pool of 10 healthy donor B cell samples.
2012-05-30 | E-GEOD-33623 | biostudies-arrayexpress
Project description:Several studies have demonstrated an impaired function of the microenvironment in chronic lymphocytic leukemia (CLL), contributing to immune evasion of tumor cells and disease progression. However, in CLL-like monoclonal B cell lymphocytosis (MBL) studies are scarce. Herein, a comprehensive characterization of the microenvironment in 59 MBL, 56 early stage CLL and 31 healthy controls was conducted. Gene expression arrays and qRT-PCR were performed on RNA from CD4+ peripheral blood cells; serum cytokines were measured by immunoassays and proteomic studies; and flow cytometry was applied to evaluate peripheral blood cytotoxic, Th1, exhausted and effector CD4+ T cells, besides monocytic CD14, CD4 and HLA-DR expression. MBL and early stage CLL showed a similar upregulation of cytotoxic and Th1-related genes, expanded perforin+ and CXCR3+ CD4+ T cells as well as PD1+ CD4+ T cells compared to controls. However, a strong inflammatory response was only identified in MBL: enhanced phagocytosis, pattern recognition receptors, IL8, HMGB1, TREM1 and acute response signaling pathways, along with increased levels of proinflammatory cytokines (remarkably IL8, IFN? and TNF?). Of note, this inflammatory drive was decreased in early stage CLL: diminished proinflammatory cytokines including IFN?, decreased IL8 signaling pathway and lower monocytic HLA-DR expression compared to MBL. Besides, this inflammation was especially reduced in IGHV mutated CLL, involving a decrease of the proinflammatory HMGB1 signaling pathway. These novel findings reveal a different pathophysiology between MBL and CLL, paving the way for the development of pre-emptive immunotherapies with optimal benefits at MBL and early stage CLL, before intense immune exhaustion.
2020-03-29 | GSE125791 | GEO