Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA373906 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Integrating genomic alterations in diffuse large B-cell lymphoma identifies new relevant pathways and potential therapeutic targets
| PRJEB19228 | ENA
Project description:Plasmablastic lymphoma is a high grade B cell lymphoma with plasmablastic morphology and a terminally differentiated B cell immunophenotype, usually arising in the setting of immunodeficiency and often demonstrating Epstein Barr Virus positivity. The molecular and genetic mechanisms underlying the pathogenesis of PBL are largely unknown. To better understand its pathogenesis, herein we have analyzed global gene expression of PBL and compared that to gene expression profiles of diffuse large B cell lymphoma. While overlaps in transcriptomes between these malignancies were identified, we have shown that the gene expression profile of plasmablastic lymphoma is distinct, demonstrating striking downregulation of B cell receptor signaling genes, BCL6, BCL11A SPI-B, targets of NFKB1, and upregulation of mitochondrial genes, PRMT5, MYC and MYC targets and IL21, implicating these alterations in the pathogenesis of this lymphoma. In addition we show the usefulness of SWAP-70 immunohistochemistry in the differentiation of immunoblastic diffuse large B cell lymphoma and plasmablastic lymphoma. Our findings provide justification for considering plasmablastic lymphoma as a specific lymphoma entity and provide insight into the unique transcriptional aberrations occurring in this high-grade lymphoma. Expression profiles of 15 plasmablastic lymphomas and 10 diffuse large B-cell lymphomas were obtained using Afymmetrix U133A2 microarrays.
2015-09-15 | E-GEOD-53117 | biostudies-arrayexpress
Project description:Diffuse large B-cell lymphoma (DLBCL) is a clinically and biologically heterogeneous disease. We have characterized recurrent copy number alterations (CNAs) in a large series of primary DLBCLs with HD-SNP arrays and the GISTIC algromithm. We evaluated the associations between transcript abundance and the presence of specific CNAs by obtaining RNA profiles on the majority of the primary DLBCLs and integrating the gene expression profiles with the copy number data.
2012-09-12 | GSE34171 | 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
2013-12-10 | E-GEOD-46663 | biostudies-arrayexpress
Project description:to screen and identify differentially expressed microRNAs (miRNAs) between diffuse large B-cell lymphoma (DLBCL) and control (lymph node reactive hyperplasia, LRH) groups, investigate whether miRNAs associated with DLBCL and could serve as potential therapeutic targets.
2021-09-22 | GSE173080 | GEO
Project description:Transcriptomics and genetic characterization of Diffuse large B-cell lymphoma (DLBCL) have increased the understanding of the pathogenesis of the disease and provided potential novel therapeutic targets. This dataset collects transcriptomic and methylation assays for 168 DLBCL tissue samples.
2021-01-21 | GSE145043 | GEO
Project description:Plasmablastic lymphoma is a high grade B cell lymphoma with plasmablastic morphology and a terminally differentiated B cell immunophenotype, usually arising in the setting of immunodeficiency and often demonstrating Epstein Barr Virus positivity. The molecular and genetic mechanisms underlying the pathogenesis of PBL are largely unknown. To better understand its pathogenesis, herein we have analyzed global gene expression of PBL and compared that to gene expression profiles of diffuse large B cell lymphoma. While overlaps in transcriptomes between these malignancies were identified, we have shown that the gene expression profile of plasmablastic lymphoma is distinct, demonstrating striking downregulation of B cell receptor signaling genes, BCL6, BCL11A SPI-B, targets of NFKB1, and upregulation of mitochondrial genes, PRMT5, MYC and MYC targets and IL21, implicating these alterations in the pathogenesis of this lymphoma. In addition we show the usefulness of SWAP-70 immunohistochemistry in the differentiation of immunoblastic diffuse large B cell lymphoma and plasmablastic lymphoma. Our findings provide justification for considering plasmablastic lymphoma as a specific lymphoma entity and provide insight into the unique transcriptional aberrations occurring in this high-grade lymphoma.
2015-09-15 | GSE53117 | GEO
Project description:Genome studies of diffuse large B-cell lymphoma (DLBCL) have revealed a large number of somatic mutations and structural alterations that may contribute to their heterogeneous behavior. However, their clinical relevance and potential interest in identifying appropriate candidate drugs for personalized management are not well known. In this study, targeted next generation sequencing and genomic copy number alterations (CNA) were analyzed in 150 cases of diffuse large B-cell lymphoma (DLBCL) to define the clinical significance of recurrent genomic alterations and to identify potential targets for personalized management. An independent cohort of 111 patients was also analyzed to confirm the clinically significant findings. We found a differential profile of mutations, altered pathogenic pathways and CNA in germinal center B (GCB) and activated B-cell (ABC)-DLBCL with some shared alterations in both subtypes. Mutations in genes of the NOTCH pathway and tumor suppressor genes (TP53/CDKN2A), but not individual genes, conferred an unfavorable prognosis that was independent of other parameters and confirmed in the validation cohort. Tumors with NOTCH pathway mutations had a significant overexpression of downstream target genes, emphasizing the relevance of this pathway in DLBCL. We identified other new relevant genes including TMEM30A, RHOA, EBF, and TOX, among others. In silico drug discovery analysis recognized 69 (46%) cases carrying at least one genomic alteration considered a potential target of drug response according to early clinical trials (n=66) or pre-clinical assays (n=3) in DLBCL or other lymphomas. These findings orient future preclinical and clinical intervention strategies in DLBCL.
2018-03-14 | GSE94705 | GEO