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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Subtype Specific Addiction of the Activated B Cell Subset of Diffuse Large B Cell Lymphoma to FOXP1

ABSTRACT: Genome wide transcript and target gene profiling reveal that FOXP1 acts directly and indirectly by enforcing known ABC-DLBCL hallmarks, including Chronically Activated B cell receptor Signaling (CABS) and the classical NF-ÎºB survival pathway. Our data further suggest that FOXP1 maintains ABC-subtype distinction by repressing gene expression programs dominant in GCB-DLBCL and support a model in which the normally transitory B cell plasmablast is the target of ABC-DLBCL transformation. ChIP sequenicng was performed for the FOXP1 transcription factor in DLBCL cell lines. Input was sequenced and used as a control.

ORGANISM(S): Homo sapiens

SUBMITTER: Vishy Iyer

PROVIDER: E-GEOD-63257 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Subtype Specific Addiction of the Activated B Cell Subset of Diffuse Large B Cell Lymphoma to FOXP1

Project description:Genome wide transcript and target gene profiling reveal that FOXP1 acts directly and indirectly by enforcing known ABC-DLBCL hallmarks, including Chronically Activated B cell receptor Signaling (CABS) and the classical NF-κB survival pathway. Our data further suggest that FOXP1 maintains ABC-subtype distinction by repressing gene expression programs dominant in GCB-DLBCL and support a model in which the normally transitory B cell plasmablast is the target of ABC-DLBCL transformation.

2016-01-03 | GSE63257 | GEO

FOXP1 in ABC DLBCL

Project description:High expression of the FOXP1 transcription factor distinguishes the highly aggressive Activated B Cell (ABC) type of Diffuse Large B Cell Lymphoma (DLBCL) from the more indolent Germinal Center (GCB) DLBCL subtype and is correlated with poor prognosis. A genetic or functional role for FOXP1 in lymphomagenesis and/or tumor maintenance, however, remains unknown. Here, we report that sustained expression of FOXP1 is necessary for ABC DLBCL cell line survival. Genome-wide transcript profiling reveals that FOXP1 acts directly and indirectly by enforcing expression of known ABC DLBCL hallmarks, including the classical NF-kappaB survival pathway. Our data further suggest that FOXP1 maintains the ABC subtype distinction by repressing gene expression programs dominant in GCB DLBCL and supports a model in which the target of ABC DLBCL transformation is a transitory cell type en route from the germinal center B cell to the terminally differentiated plasma cell.

2015-12-01 | GSE64586 | GEO

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2015-10-27 | E-GEOD-71526 | biostudies-arrayexpress

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Dendritic Cell Fate is Determined by BCL11A

Project description:Here we confirm an essential requirement for the BCL11A transcription factor in fetal pDC development, and for the first time demonstrate this lineage specific requirement in the adult organism. Genome-wide analyses of BCL11A DNA binding and expression revealed that BCL11A regulates transcription of E2-2 and other pDC differentiation modulators including ID2 and MTG16. Our results identify BCL11A as an essential, lineage-specific factor that regulates pDC development. ChIP sequenicng was performed for a transcription factor of BCL11A in Cal1 cell line. Input was sequenced and used as a control.

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Homo sapiens

Project description:FOXP1 in ABC DLBCL

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Transcriptional profiling of human OCI-Ly1 DLBCL cells after siRNA-mediated silencing of FOXP1 [array]

Project description:We have developed a novel immunocompetent multi-lesion mouse model of activated B cell diffuse large B-cell lymphoma (ABC-DLBCL; the pBIC mice) that recapitulates relatively fast the molecular, cellular and tumor microenvironment of aggressive human ABC-DLBCL. We demonstrate that perturbed p53 signaling cooperates with constitutive NF-kB activation in GC-experienced plasmablasts with blocked terminal differentiation to promote lymphomagenesis and tumor progression through triggering downstream intracellular molecular addictions (e.g. deregulating Foxp1 and AID pathways) and intercellular immunosuppressive signals for evading anti-tumoral responses (e.g. MHC-II antigen presentation and deregulating PD-L1/PD-1 immune checkpoint). Our immunocompetent ABC-DLBCL murine model provides in vivo evidence that PD-1 blockade cooperates with anti-CD20-based current standard-of-care therapy to reshape the immunosuppressive TME and facilitate long-term anti-tumoral responses. Therefore, our results support that immune checkpoints may hold promising therapeutic potential in ABC-DLBCL.

2019-04-19 | GSE116289 | GEO

Elucidation of FOXP1 target genes in DLBCL by RNA-Seq

Project description:Elucidation of FOXP1 target genes by RNA-Seq of DLBCL cell lines transfected with siRNAs targeting FOXP1 expression

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EGR1 addiction in diffuse large B cell lymphoma

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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

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