Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA218584 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR974993.fastq.gz | Fastqsanger.gz | |||
| SRR974994.fastq.gz | Fastqsanger.gz | |||
| SRR974995.fastq.gz | Fastqsanger.gz | |||
| SRR974996.fastq.gz | Fastqsanger.gz | |||
| SRR974997.fastq.gz | Fastqsanger.gz |
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Project description:The goal of this study is to identify the effect of the transcription factor STAT3 in the two major subtypes of diffuse large B cell lymphoma (DLBCL). STAT3 is a signal transducer that, when dysregulated, becomes a powerful oncogene found in many human cancers, including DLBCL. DLBCL is the most common form of non-Hodgkin’s lymphoma and has two major subtypes: germinal center B-cell-like (GCB) and activated B-cell-like (ABC). When compared to the GCB form, ABC lymphomas respond much more poorly to current therapies and often exhibit overexpression or overactivation of STAT3. To investigate how STAT3 might contribute to this aggressive phenotype, we have used ChIP-Seq to identify STAT3 binding sites in 8 DLBCL cell lines (4 GCB subtype, 4 ABC) that are derived from patient tumors. 10,337 distinct STAT3 binding regions are occupied in at least two of the eight cell lines. One third (n = 3524) are differentially bound by STAT3 between the two subtypes (FDR < 0.05). More BRs are strongly bound in ABC than in GCB: 44% of differentially bound BRs (n = 1550) show more STAT3 binding in GCB, while 56% (n = 1974) are more strongly bound in ABC. Identification and comparison of STAT3 transcription factor binding sites in 8 cell lines that represent the 2 subtypes of DLBCL. 4 cell lines are subtyped as ABC and 4 are subtyped as GCB. 2-9 replicates and 1 input control are present for each cell line. (Cell line OCI-Ly19 was not included in the final analysis because RNA-Seq showed that its gene expression clustered in between the subtypes, probably due to its EBV+ status. However, its peak calls were used in intermediate steps of the analysis pipeline. Its sequencing runs have been included for completeness.)
2013-12-16 | E-GEOD-50723 | biostudies-arrayexpress
Project description:The goal of this study is to identify the effect of the transcription factor STAT3 in the two major subtypes of diffuse large B cell lymphoma (DLBCL). STAT3 is a signal transducer that, when dysregulated, becomes a powerful oncogene found in many human cancers, including DLBCL. DLBCL is the most common form of non-Hodgkin’s lymphoma and has two major subtypes: germinal center B-cell-like (GCB) and activated B-cell-like (ABC). When compared to the GCB form, ABC lymphomas respond much more poorly to current therapies and often exhibit overexpression or overactivation of STAT3. To investigate how STAT3 might contribute to this aggressive phenotype, we have used ChIP-Seq to identify STAT3 binding sites in 8 DLBCL cell lines (4 GCB subtype, 4 ABC) that are derived from patient tumors. 10,337 distinct STAT3 binding regions are occupied in at least two of the eight cell lines. One third (n = 3524) are differentially bound by STAT3 between the two subtypes (FDR < 0.05). More BRs are strongly bound in ABC than in GCB: 44% of differentially bound BRs (n = 1550) show more STAT3 binding in GCB, while 56% (n = 1974) are more strongly bound in ABC.
2013-12-16 | GSE50723 | GEO
Project description:Whole transcriptome profiling of the two major subtypes of diffuse large B cell lymphoma
| PRJNA218585 | ENA
Project description:Correlation between STAT3 binding presence and gene expression levels in subtypes of diffuse large B cell lymphoma
| PRJNA218583 | ENA
Project description:Diffuse large B-cell lymphoma (DLBCL) is the most common non-Hodgkin lymphoma, including two main molecular subtypes termed activated B cell-like (ABC) and germinal center B cell-like (GCB). ABC DLBCL is less curable and identification of new molecular targets is needed for the development of effective therapeutic agents. Here, we focused on EGR1, a transcription factor that is regulated by the B cell receptor and JAK1/STAT3 signaling pathway in ABC DLBCL. ChIP-Seq and RNA-Seq analyses revealed that gene regulation by EGR1 in ABC DLBCL accentuates multiple oncogenic pathways, including MYC and E2F, while dampening the lethal type I IFN pathway.
2021-08-06 | GSE123291 | GEO
Project description:Diffuse large B cell lymphoma (DLBCL), the most common non-Hodgkin lymphoma, includes two main molecular subtypes: activated B cell-like (ABC) DLBCL and germinal center B cell-like (GCB) DLBCL. ABC DLBCL is more aggressive, with the activated JAK1-STAT3 pathway that promotes cell survival. In order to study the underlying pathogenic mechanism, we performed a ChIP-seq experiment by phospho-STAT3(Tyr705) antibody in ABC DLBCL cell lines, and identified 3,456 STAT3 target genes genome-wide. In parallel, ChIP-seq experiment was performed with STAT3 antibody in α-IgM stimulated naïve B cells for verification of these targets of STAT3 protein. TMD8 was treated by eithor DMSO or AZD1480 (JAK inhibitor) for 4hrs, ChIP-seq experiments were performed by pSTAT3(Tyr705) antibody (#9145S, Cell signaling). Naïve B cells were collected from peripheral blood mononuclear cells by Naive B Cell Isolation kit (miltenyi biotec; 130-091-150), and treated by 10ug/ml α-IgM (southernbiotech; #2020-01) for 24hrs. ChIP-seq experiments were performed by STAT3 antibody (SC-482X, Santa Cruz).
2019-05-01 | GSE123398 | GEO
Project description:Diffuse large B-cell lymphoma (DLBCL) is currently divided into three main molecular subtypes, defined by gene expression profiling (GEP): Germinal Center B-cell like (GCB), Activated B-Cell like (ABC), and Primary Mediastinal B-cell Lymphoma (PMBL). DLBCL subtypes were determined according to patients' gene expression profiles.
2017-01-30 | GSE87371 | GEO
Project description:Multi-agent chemotherapy still represents the first-line standard-of-care treatment for diffuse large B-cell lymphoma (DLBCL), the most common form of lymphoma in adults. However, the clinicopathological and molecular heterogeneity of DLBCLs poses a major challenge in their successful therapy. At least two major subtypes, i.e. germinal center B-cell-like (GCB) and the aggressive activated B-cell-like (ABC) DLBCL, which differ both in their gene expression profile and in their mutation patterns, have been identified. Here we demonstrate a broad inhibitory effect of dimethyl fumarate (DMF) on the outgrowth of both DLBCL subtypes, even though the molecular basis for its efficacy differs between GCB and ABC DLBCL. Due to high expression of arachidonate 5-lipoxygenase in concert with low glutathione and glutathione peroxidase 4 levels, DMF induced lipid peroxidation and thus ferroptotic cell death in GCB DLBCL. In contrast, in ABC DLBCL inhibition of NF-κB and STAT3 activity essentially contributed to DMF-dependent cytotoxicity. Interestingly, the BCL-2 specific BH3 mimetic ABT-199 or an inhibitor of the ferroptosis suppressor protein 1 synergized with DMF treatment in inducing cell death in DLBCL cell lines. Collectively, our findings identify the established and approved drug DMF as a promising novel therapeutic option in the treatment of both GCB and ABC DLBCL.
2021-07-01 | GSE164267 | GEO