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Genome-wide Detection of Genes Targeted by Aberrant Somatic Hypermutation in Lymphoma

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE34316 | GEO | 2012/07/16

SECONDARY ACCESSION(S): PRJNA151499

REPOSITORIES: GEO

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Genome-wide Detection of Genes Targeted by Aberrant Somatic Hypermutation in Lymphoma

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

Microarray expression profile of long noncoding RNAs in germinal center-like diffuse large B-cell lymphoma cell lines.

Project description:The contributions of long noncoding RNAs (lncRNAs) to the development of germinal center (GCB)-like diffuse large B-cell lymphoma (DLBCL) remain largely unknown. The aim of this study was to investigate the expression profile of lncRNAs in human GCB DLBCL cell lines (OCI-ly1 and OCI-ly19) and normal B lymphocytes by microarray. We demonstrated that 21,539 lncRNAs were expressed in all samples analyzed, of which 1,648 lncRNAs were upregulated and 2,671 lncRNAs were downregulated in GCB DLBCL cell lines (OCI-ly1 and OCI-ly19) (≥2.0-fold, P<0.05).

2019-01-01 | GSE97336 | GEO

Recruitment of FOXP1 to target genes in diffuse large B-cell lymphoma (DLBCL) cells

Project description:Identification of FOXP1 target genes in the OCI-Ly1 DLBCL cell line by ChIP-on-chip Three replicates of the FOXP1 ChIP-on-chip were performed in the OCI-Ly1 cells

2013-05-03 | E-GEOD-44243 | biostudies-arrayexpress

Recruitment of FOXP1 to target genes in diffuse large B-cell lymphoma (DLBCL) cells

Project description:Identification of FOXP1 target genes in the OCI-Ly1 DLBCL cell line by ChIP-on-chip

2013-05-03 | GSE44243 | GEO

Gene expression signatures for Ibrutinib resistance in Diffuse Large B-cell Lymphoma (ABC-DLBCL)

Project description:To understand the acquired resistance mechanism in DLBCL the cell lines (OCI-Ly1, Oci-Ly10 and HBL-1) were treated with Ibrutinib over time to generate resistant clone.

2019-11-01 | GSE138126 | GEO

Retroviral overexpression or siRNA mediated knockdown of FOXP1 in DLBCL cell lines and primary human B cells

Project description:To provide insight into the role of and target genes of the transcription factor FOXP1 in mature human B cells and in B cell non-Hodkgin lymhomas, we performed gene expression microarray studies, upon ectopic overexpression or silencing of FOXP1 in these cells. human memory B cells from 2 separate donors were transduced with LZRS-FOXP1-IRES-YFP or LZRS-IRES-YFP (negative control); DLBCL cell lines OCI-Ly1, OCI-Ly7, and OCI-Ly10 were transduced with LZRS-FOXP1-IRES-YFP or LZRS-IRES-YFP (negative control); DLBCL cell lines OCI-Ly1, OCI-Ly7, and OCI-Ly10 were transiently transfected with siRNA targeting FOXP1 or sigenome non-targeting siRNA (negative control), using the Lonza nucleofection system.

2014-10-24 | E-GEOD-51382 | biostudies-arrayexpress

Time course gene expression profiling of five diffuse large B-cell lymphoma cell lines following JQ1 treatment

2013-12-10 | GSE45630 | GEO

Time course gene expression profiling of five diffuse large B-cell lymphoma cell lines following JQ1 treatment

Project description:To understand the molecular curcuits perturbed by BET bromodoman inhibtion we obtained gene expression profiling of five DLBCL cell lines, SU-DHL6, OCI-Ly1, OCI-Ly4, Toledo and HBL-1, which were treated with either 500nM JQ1 or DMSO for 0,2,6,12,24 and 48hr. RNA samples from five DLBCL cell lines at baseline (time 0) or following treatment with 500nM of JQ1 or vehicle (DMSO) alone for 2, 6, 24 or 48 hours were profiled in triplicate on Affymetrix Human Gene 1.0 ST Array.

2013-12-10 | E-GEOD-45630 | biostudies-arrayexpress

CDK9 inhibition with AZD4573 in DLBCL

Project description:We report the effects of CDK9 inhibition (AZD4573) on the epigenetic landscape in Diffuse Large B-cell Lymphoma (DLBCL). This study utilized chromatin immunoprecipitation with massively parallel DNA sequencing (ChIP-seq) to assess genome-wide post-translational histone modifications (H3K27ac and H3K4me3) and DNA occupancy of transcriptional proteins (RNAPII and BRD4) in two DLBCL cell lines, OCI-LY3 and VAL, treated with the CDK9 inhibitor AZD4573 (30 nM). Cells were treated for 0, 3 and 8 hours prior to harvest. After 8-hour exposure, drug was washed out and cells were harvested after 24 hours. We found that CDK9 inhibition led to an increase in RNAPII promoter proximal pausing, and increase in BRD4 enrichment on the promoter, and a decrease in promoter H3K4me3. Treatment induced reprograming of the super-enhancer landscape including loss of super-enhancers next to genes in oncogenic pathways.

2022-08-05 | GSE210372 | GEO

Identification of MLL2 regulated genes in germinal center B cells

Project description:Somatic mutations of the MLL2 methyltransferase gene represent a common genetic lesion in multiple cancer types. In diffuse large B cell lymphoma (DLBCL) and follicular lymphoma (FL), these mutations are highly recurrent and occur early during tumorigenesis, suggesting a central role in transformation. Here we show that FL/DLBCL-associated MLL2 mutations impair its enzymatic activity and lead to diminished global H3K4 methylation in germinal center (GC) B cells and DLBCL, consistent with the enrichment of MLL2 binding at enhancer and promoter regions marked by mono- and tri-methylation. Conditional deletion of Mll2 early during B cell development, but not after initiation of the GC reaction, leads to an increase in GC B cells, whose transcriptional profile is enriched in cell-cycle regulatory and B-cell receptor signaling genes. Consistently, Mll2-deficient B cells exhibit proliferative advantage ex vivo. Loss of Mll2 combined with BCL2 deregulation, mimicking FL/DLBCL pathogenesis, leads to an increased incidence of clonal lymphoproliferations resembling the features of the human tumors. These findings suggest that early MLL2 loss facilitates lymphomagenesis by remodeling the epigenetic landscape of the cancer precursor cells. Eradication of MLL2-deficient cells may represent a rational therapeutic approach targeting early tumorigenic events. ChIP-seq analysis of MLL2 bound regions and histone methylation (H3K4me3, H3K4me1) in normal human germinal center B cells.

2015-09-10 | E-GEOD-67494 | biostudies-arrayexpress

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