Super-Enhancer Hypermutation Alters Oncogene Expression in B-cell Lymphoma
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ABSTRACT:
PROVIDER: PRJNA855230 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-07-03 | GSE207395 | GEO
Project description:We report a novel approach to identify genome-wide somatic hypermutation hotspots from short Illumina H3K4me3 ChIPseq reads in diffuse large B-cell lymphoma cells (DLBCL). Abberant somatic hypermation are known to occur at the promoters of several proto-oncogenes in DLBCL. To identify such events genome-wide, we performed H3K4me3 ChIPseq experiments (as to enrich promoter sequences of actively transcribed genes) in 2 DLBCL cells lines (OCI-Ly1 and OCI-Ly8) and their normal B-cell counterparts, Naive B cells (NBC) and Germinal Center B cells (GCBs). We discover new genes that harbor mutations in their promoter regions that are potentially introduced by the aberrant activation-induced cytosine deaminase activity in lymphoma cell lines, and many of these genes are important for the B cell biology. Moreover, we show that these mutations can affect the activities of these promoters. Our study provides a feasible approach for the detection of promoter mutations and broadens our knowledge on promoter mutations in lymphomas. Examination of 1 histone mark (H3K4me3) in 4 different cell types.
2012-07-16 | E-GEOD-34316 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE25636: A mouse model of deregulation of the malt1 oncogene recapitulates the pathogenesis of human malt lymphoma [MouseSca1 dataset] GSE25637: A mouse model of deregulation of the malt1 oncogene recapitulates the pathogenesis of human malt lymphoma [Spleen dataset] GSE25638: A mouse model of deregulation of the malt1 oncogene recapitulates the pathogenesis of human malt lymphoma [MALT dataset] Refer to individual Series
2012-07-09 | E-GEOD-25639 | biostudies-arrayexpress
Project description:We report a novel approach to identify genome-wide somatic hypermutation hotspots from short Illumina H3K4me3 ChIPseq reads in diffuse large B-cell lymphoma cells (DLBCL). Abberant somatic hypermation are known to occur at the promoters of several proto-oncogenes in DLBCL. To identify such events genome-wide, we performed H3K4me3 ChIPseq experiments (as to enrich promoter sequences of actively transcribed genes) in 2 DLBCL cells lines (OCI-Ly1 and OCI-Ly8) and their normal B-cell counterparts, Naive B cells (NBC) and Germinal Center B cells (GCBs). We discover new genes that harbor mutations in their promoter regions that are potentially introduced by the aberrant activation-induced cytosine deaminase activity in lymphoma cell lines, and many of these genes are important for the B cell biology. Moreover, we show that these mutations can affect the activities of these promoters. Our study provides a feasible approach for the detection of promoter mutations and broadens our knowledge on promoter mutations in lymphomas.
2012-07-16 | GSE34316 | GEO
Project description:Diffuse Large B-Cell Lymphoma (DLBCL) is a biologically heterogeneous and clinically aggressive disease. Here, we explore the role of BET bromodomain proteins in DLBCL, using integrative chemical genetics and functional epigenomics. We observe highly asymmetric loading of BRD4 at enhancers, with approximately 33% of all BRD4 localizing to enhancers at 1.6% of occupied genes. These super-enhancers prove particularly sensitive to bromodomain inhibition, explaining the selective effect of BET inhibitors on oncogenic and lineage-specific transcriptional circuits. Functional study of genes marked by super-enhancers identifies DLBCLs dependent on OCA-B and suggests a strategy for discovering unrecognized cancer dependencies. Translational studies performed on a comprehensive panel of DLBCLs establish a therapeutic rationale for evaluating BET inhibitors in this disease. ChIP-Seq for various transcription factors and histone modifications in diffuse large B-cell lymphoma cells
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Project description:H3K27ac HiChIP and ChIP-seq to identify super enhancers inprimary effusion lymphoma cell lines (PEL)
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Project description:Correct classification of cancer patients into subtypes is a prerequisite for acute diagnosis and effective treatment. Currently this classification relies mainly on histological assessment, but gene expression analysis bymicroarrays has shown great promise. Here we show that high accuracy, quantitative proteomics can robustly segregate cancer subtypes directly at the level of expressed proteins. We investigated two histologically indistinguishable subtypes of diffuse large B-cell lymphoma (DLBCL): activated Bcell- like (ABC) and germinal-center B-cell-like (GCB) subtypes, by first developing a general lymphoma stable isotope labeling with amino acids in cell culture (SILAC) mix from heavy stable isotope-labeled cell lines. This super- SILAC mix was combined with cell lysates from five ABCDLBCL and five GCB-DLBCL cell lines. Shotgun proteomic analysis on a linear ion trap Orbitrap mass spectrometer with high mass accuracy at the MS and MS/MS levels yielded a proteome of more than 7,500 identified proteins. High accuracy of quantification allowed robust separation of subtypes by principal component analysis. The main contributors to the classification included proteins known to be differentially expressed between the subtypes such as the transcription factors IRF4 and SPI1/ PU.1, cell surface markers CD44 and CD27, as well as novel candidates. We extracted a signature of 55 proteins that segregated subtypes and contained proteins connected to functional differences between the ABC and GCB-DLBCL subtypes, including many NF-kappa B-regulated genes. Shortening the analysis time to single-shot analysis combined with use of the new linear quadrupole Orbitrap analyzer (Q Exactive) also clearly differentiated between the subtypes. These results show that high resolution shotgun proteomics combined with super-SILAC-based quantification is a promising new technology for tumor characterization and classification.
2015-04-24 | PXD002098 | Pride
Project description:This SuperSeries is composed of the following subset Series: GSE39108: UNG shapes the specifity of AID-induced somatic hypermutation in non B cells GSE39114: UNG shapes the specifity of AID-induced somatic hypermutation in B cells Refer to individual Series
2012-07-04 | E-GEOD-39115 | biostudies-arrayexpress
Project description:Here we apply integrated epigenomic and transcriptomic profiling to uncover super-enhancer heterogeneity between breast cancer subtypes, and provide clinically relevant biological insights towards TNBC. Using CRISPR/Cas9-mediated gene editing, we identify genes that are specifically regulated by TNBC-specific super-enhancers, including FOXC1 and MET, thereby unveiling a mechanism for specific overexpression of the key oncogenes in TNBC. We also identify ANLN as a novel TNBC-specific gene regulated by super-enhancer. Our studies reveal a TNBC-specific epigenomic landscape, contributing to the dysregulated oncogene expression in breast tumorigenesis.
2021-03-04 | PXD024505 | iProX