Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling in B220+ from normal spleen, VavPBcl2/vector and VavPBcl2/Myc lymphomas

ABSTRACT: Follicular lymphoma (FL) is the second most common forms of B cell lymphoma that result from the expansion of germinal center (GC) B cells. Here, we aimed to find differential expression of genes between noemal spleen, indoent FL (VavPBcl2/vector) and transformed and aggressive FL (VavPBcl2/MYC) in our mouse model.

ORGANISM(S): Mus musculus

PROVIDER: GSE142335 | GEO | 2019/12/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiling in follicular lymphoma (FL) samples and paired transformed follicular lymphoma (tFL) (n=6 samples)

Project description:Follicular lymphoma (FL) is the second most common forms of B cell lymphoma that result from the expansion of germinal center (GC) B cells. Here, we aimed to find differential expression of genes between patient samples isolated from indoent FL or transformed and aggressive FL.

2019-12-20 | GSE142334 | GEO

Array based comparative genomic hybridisation analysis of 1 Mb resolution of 21 follicular lymphomas (FL), 31 transformed diffuse large B-cells lymphomas (DLBCL), 29 de novo DLBCL (10 of GC and 19 non-GC related immunophenotype).

Project description:Follicular lymphoma (FL) is one of the most common types of indolent B-cell lymphoma in Western countries. FL commonly transforms to more aggressive diffuse large B-cell lymphoma (DLBCL) at reported frequencies between 15 - 60%. We have used microarray comparative genomic hybridisation (aCGH) at 1 Mb resolution to study copy number changes in paired tumor samples (primary FL and a subsequent tDLBCL) as well as de novo DLBCL cases to outline genetic mechanisms of transformation from follicular lymphoma to diffuse large B-cell lymphoma. Single hybridization per case. 21 FL, 31 transformed DLBCL, 29 de novo DLBCL (10 GC and 19 non-GC DLBCL). Tumor labelled with Cy5 and reference with Cy3. Mixture of 20 normal male or female genomic DNA was used in sex-mismatched hybridization.

2014-04-18 | E-GEOD-56884 | biostudies-arrayexpress

Enhancer Sequence Variants and Transcription Factor Deregulation Synergize to Construct Pathogenic Regulatory Circuits in B Cell Lymphoma (RNA-Seq)

Project description:Most B cell lymphomas arise in the germinal center (GC), where humoral immune responses evolve from potentially oncogenic cycles of mutation, proliferation, and clonal selection. Although lymphoma gene expression diverges significantly from GC-B cells, underlying mechanisms that alter the activities of corresponding regulatory elements (REs) remain elusive. Here we define the complete pathogenic circuitry of human follicular lymphoma (FL), which activates or decommissions transcriptional circuits from normal GC-B cells and commandeers enhancers from other lineages. Moreover, independent sets of transcription factors, whose expression is deregulated in FL, target commandeered versus decommissioned REs. Our approach reveals two distinct subtypes of low-grade FL, whose pathogenic circuitries resemble GC-B or activated B cells. Remarkably, FL-altered enhancers also are enriched for sequence variants, including somatic mutations, which disrupt transcription factor binding and expression of circuit-linked genes. Thus, the pathogenic regulatory circuitry of FL reveals distinct genetic and epigenetic etiologies for GC-B transformation. Expression profiles of follicular lymphoma, centrocyte and peripheral blood B cells were generated by deep sequencing, using Illumina Hi-Seq 2000.

2015-01-15 | E-GEOD-62241 | biostudies-arrayexpress

Enhancer Sequence Variants and Transcription Factor Deregulation Synergize to Construct Pathogenic Regulatory Circuits in B Cell Lymphoma (ChIP-Seq, FAIRE-Seq)

Project description:Most B cell lymphomas arise in the germinal center (GC), where humoral immune responses evolve from potentially oncogenic cycles of mutation, proliferation, and clonal selection. Although lymphoma gene expression diverges significantly from GC-B cells, underlying mechanisms that alter the activities of corresponding regulatory elements (REs) remain elusive. Here we define the complete pathogenic circuitry of human follicular lymphoma (FL), which activates or decommissions transcriptional circuits from normal GC-B cells and commandeers enhancers from other lineages. Moreover, independent sets of transcription factors, whose expression is deregulated in FL, target commandeered versus decommissioned REs. Our approach reveals two distinct subtypes of low-grade FL, whose pathogenic circuitries resemble GC-B or activated B cells. Remarkably, FL-altered enhancers also are enriched for sequence variants, including somatic mutations, which disrupt transcription factor binding and expression of circuit-linked genes. Thus, the pathogenic regulatory circuitry of FL reveals distinct genetic and epigenetic etiologies for GC-B transformation. Molecular profiling of follicular lymphoma, resting peripheral blood and tonsillar B cells using Formaldehyde-Assisted Isolation of Regulatory Elements (FAIRE) and chromatin immunoprecipitation (H3ac and H3K27ac).

2015-01-15 | E-GEOD-62245 | biostudies-arrayexpress

Gene expression Profiling in Follicular Lymphomas

2014-07-01 | GSE55267 | GEO

Integrative single-cell analysis reveals human germinal center dynamics de-synchronized in B cell lymphoma

Project description:Most adult B cell lymphomas originate from germinal center (GC) B cells but it is unclear to what extent overt lymphoma B cells retain GC B cell functional dynamics or are blocked in a particular stage of the GC reaction. Here, we used integrative single-cell analysis of phenotype, gene expression and IGH sequence to track the characteristic human GC B cell program in follicular lymphoma (FL) B cells. By modeling the cyclic continuum of GC B cell transitional states, we identified characteristic patterns of synchronously expressed gene clusters. GC-specific gene expression synchrony was lost in single lymphoma B cells. Yet, distinct FL-specific cell states co-existed within single patient biopsies. Our data show that lymphoma B cells are not blocked in a GC B cell state but may adopt new dynamic modes of functional diversity, opening novel definitions of lymphoma identity.

2018-06-15 | GSE115795 | GEO

Gene expression profiling in RagC T89N germinal center B cells and RagC S74C murine B220+ lymphoma cells

Project description:Gene expression by RNAseq in murine germinal centers induced by SRBC in RagC T89N mice (YRT codes) and RNAseq in murine B220+ from VavVPBcl2/RagC S74C and VavVPBcl2/RagC +/+ lymphomas Follicular Lymphoma (FL) is an incurable B cell malignancy derived from germinal center (GC) B cells. The RRAGC gene, encoding a GTPase that links cellular nutrient sufficiency with the activation of mechanistic target of rapamycin complex 1 (mTORC1) is mutated in 15% of FL patients, but its impact in B cell functions and lymphomas is unexplored. Endogenous expression of Rragc mutant variants in B lymphocytes from novel knock-in strains of mice resulted in a partial insensitivity of mTORC1 to nutrient deprivation. A mild, but not a full-blown activation of the nutrient signaling pathway enhanced B cell activation and the GC response, suppressed apoptosis, and accelerated lymphomagenesis. Moreover, murine RRAGC mutant FL showed selective vulnerability to pharmacological inhibition of mTORC1. This moderate increase in nutrient signaling synergized with paracrine cues from the supportive T cell microenvironment that activate mTORC1 via the PI3K-Akt axis to promote B cell activation. Hence, RRAGC mutations sustained experimental GCs and murine and human FL in the presence of decreased T cell support. Moreover, mutations in RRAGC in human FLs are mutually-exclusive with mutations that result in increased abundance of T helper cells, consistent with functional redundancy between those pathways. Taken together, our results support a model in which activating mutations in the nutrient signaling pathway foster lymphomagenesis by corrupting a nutrient-dependent control of mTORC1-activating paracrine signals from the T cell microenvironment

2019-07-15 | GSE125394 | GEO

Gene expression Profiling in Follicular Lymphomas

Project description:Follicular lymphoma (FL) is an indolent, but incurable subtype of non-Hodgkin lymphoma. These tumor harbor t (14;18) translocation in at least 90% of patients. Recently, activating EZH2 mutations have been Follicular lymphoma (FL) is an indolent, but incurable subtype of non-Hodgkin lymphoma. These tumor harbor t (14;18) translocation in at least 90% of patients. Recently, activating EZH2 mutations have been found in a significant number of patients with FL. Gene expression profiling (GEP) was performed to determine differential gene-expression between the EZH2 mutated vs unmutated subgroups in FL. Total RNA extracted from fresh frozen specimens with FL diagnosis were processed for hybridization to Affymetrix HG-U133 plus 2 arrays. To enhance the identification of differential gene expression in FL tumor cells only, FL cases with a high B-cell content (enriched B-cell signature of >2-fold above the mean of the B-cell signature (pan B-cell markers) in the entire FL data set) were chosen for analysis.

2014-07-01 | E-GEOD-55267 | biostudies-arrayexpress

Enhancer Sequence Variants and Transcription Factor Deregulation Synergize to Construct Pathogenic Regulatory Circuits in B Cell Lymphoma (RNA-Seq)

2015-01-15 | GSE62241 | GEO

Enhancer Sequence Variants and Transcription Factor Deregulation Synergize to Construct Pathogenic Regulatory Circuits in B Cell Lymphoma (array)

2015-01-15 | GSE61912 | GEO