Whole-transcript expression data from normal and DLBCL human peripheral blood samples
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE83632 | GEO | 2016/07/06
SECONDARY ACCESSION(S): PRJNA326532
REPOSITORIES: GEO
Similar Datasets
Project description:Gene expression profiling based classification of DLBCL patients versus healthy donors provides insights on transcriptional regulation processes. Within the most represented pathways in DLBCL, we identified an innate immune response signature, as well as an anti-inflammatory response. On the other hand, a significant under-representation of pathways involved in T-cell activation was also revealed. Whole blood from 76 DLBCL patients and 87 healthy donors was collected into PAXgene Blood RNA tubes (Becton Dickinson BD Biosciences, San Jose, CA, USA) ensuring blood stabilization and stored at -80°C before RNA extraction. Total RNA, after globin mRNA depletion, was hybridized onto Affymetrix GeneChip® Human Exon 1.0 ST oligonucleotide arrays (Affymetrix, Santa Clara, CA, USA) according to manufacturerâs instructions.
2016-07-06 | E-GEOD-83632 | biostudies-arrayexpress
Project description:Diffuse large B-cell lymphoma (DLBCL) is the most common form of lymphoma in adults. The disease exhibits a striking heterogeneity in gene expression profiles and clinical outcomes, but its genetic causes remain to be fully defined. Through whole genome and exome sequencing, we characterized the genetic diversity of DLBCL. In all, we sequenced 73 DLBCL primary tumors (34 with matched normal DNA). Separately, we sequenced the exomes of 21 DLBCL cell lines. We identified 322 DLBCL cancer genes that were recurrently mutated in primary DLBCLs. We identified recurrent mutations implicating a number of known and not previously identified genes and pathways in DLBCL including those related to chromatin modification (ARID1A and MEF2B), NF-κB (CARD11 and TNFAIP3), PI3 kinase (PIK3CD, PIK3R1, and MTOR), B-cell lineage (IRF8, POU2F2, and GNA13), and WNT signaling (WIF1). We also experimentally validated a mutation in PIK3CD, a gene not previously implicated in lymphomas. The patterns of mutation demonstrated a classic long tail distribution with substantial variation of mutated genes from patient to patient and also between published studies. Thus, our study reveals the tremendous genetic heterogeneity that underlies lymphomas and highlights the need for personalized medicine approaches to treating these patients. 21 DLBCL cell lines and 70 DLBCL patient samples.
2013-01-23 | E-GEOD-43606 | biostudies-arrayexpress
Project description:We performed array comparative genomic hybridization (aCGH) and gene expression profiling in 203 samples of diffuse large B cell lymphoma (DLBCL). By gene expression, at least three molecular subtypes of DLBCL termed as germinal center B cell-like (GCB) DLBCL, activated B cell-like (ABC) DLBCL, and primary mediastinal B cell lymphoma (PMBL) can be distinguished. Combining gene expression profiling and aCGH, revealed copy number abnormalities that had strikingly different frequencies in the three molecular DLBCL subtypes. These data provide genetic evidence that the DLBCL subtypes are distinct diseases that utilize different oncogenic pathways. Keywords: clinical history design The retrospective study included RNA and DNA extracted from 203 clinical samples.
2008-09-04 | E-GEOD-11318 | biostudies-arrayexpress
Project description:We performed array comparative genomic hybridization (aCGH) and gene expression profiling in 203 samples of diffuse large B cell lymphoma (DLBCL). By gene expression, at least three molecular subtypes of DLBCL termed as germinal center B cell-like (GCB) DLBCL, activated B cell-like (ABC) DLBCL, and primary mediastinal B cell lymphoma (PMBL) can be distinguished. Combining gene expression profiling and aCGH, revealed copy number abnormalities that had strikingly different frequencies in the three molecular DLBCL subtypes. These data provide genetic evidence that the DLBCL subtypes are distinct diseases that utilize different oncogenic pathways. Keywords: clinical history design
2008-09-04 | GSE11318 | GEO
Project description:Diffuse large B-cell lymphoma (DLBCL) is the most common form of lymphoma in adults. The disease exhibits a striking heterogeneity in gene expression profiles and clinical outcomes, but its genetic causes remain to be fully defined. Through whole genome and exome sequencing, we characterized the genetic diversity of DLBCL. In all, we sequenced 73 DLBCL primary tumors (34 with matched normal DNA). Separately, we sequenced the exomes of 21 DLBCL cell lines. We identified 322 DLBCL cancer genes that were recurrently mutated in primary DLBCLs. We identified recurrent mutations implicating a number of known and not previously identified genes and pathways in DLBCL including those related to chromatin modification (ARID1A and MEF2B), NF-κB (CARD11 and TNFAIP3), PI3 kinase (PIK3CD, PIK3R1, and MTOR), B-cell lineage (IRF8, POU2F2, and GNA13), and WNT signaling (WIF1). We also experimentally validated a mutation in PIK3CD, a gene not previously implicated in lymphomas. The patterns of mutation demonstrated a classic long tail distribution with substantial variation of mutated genes from patient to patient and also between published studies. Thus, our study reveals the tremendous genetic heterogeneity that underlies lymphomas and highlights the need for personalized medicine approaches to treating these patients.
2013-01-23 | GSE43606 | GEO
Project description:We report that in absence of ATM signaling SIRT3 stimluated pathways are critical for development of DLBCL
2020-12-09 | GSE145359 | GEO
Project description:Diffuse large B-cell lymphoma (DLBCL) is the most frequent entity among non-Hodgkin lymphoma (NHL). It is a clinically and biologically heterogeneous disease regarding treatment response and long-term outcome. The anthracycline-based regimen R-CHOP is still considered as the standard of care for first-line treatment allowing achieving a complete response for approximately 60% of the patients. The prognosis of patients with primary refractory or relapsed (R/R) disease is particularly poor with a median overall survival below one year. Only a fraction of R/R patients can be cured with salvage therapies due to the acquisition of chemoresistance. We conducted a large-scale and deep proteomic investigation of the proteome profiles of R/R DLBCL patients compared to chemosensitive patients in order to identify new potential biomarkers related to resistance to treatment and to better understand the biological mechanisms underlying chemoresistance.
2019-03-04 | PXD009089 | Pride
Project description:Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) is an indolent lymphoma, but can transform into diffuse large B cell lymphoma (DLBCL), showing a more aggressive clinical behavior. Little is known about these cases on the molecular level. Therefore, the aim of the present study was to characterize DLBCL transformed from NLPHL (LP-DLBCL) by gene expression profiling (GEP). GEP revealed an inflammatory signature pinpointing to a specific host response. In a coculture model resembling this host response, DEV tumor cells showed an impaired growth behavior. Mechanisms involved in the reduced tumor cell proliferation included a downregulation of MYC and its target genes. Lack of MYC expression was also confirmed in 12/16 LP-DLBCL by immunohistochemistry. Furthermore, CD274/PD-L1 was upregulated in tumor cells after coculture with T cells or monocytes and its expression was validated in 12/19 cases of LP-DLBCL. Thereby, our data provide new insights into the pathogenesis of LP-DLBCL and a concrete explanation of the relatively low tumor cell content. Moreover, our results suggest that treatment of these patients with checkpoint inhibitors may enhance an already ongoing host response in these patients.
2017-06-12 | GSE84464 | GEO
Project description:Genomic profiles of DLBCL (Diffuse Large B-cell Lymphoma) patients 20 DLBCL patients were selected for detection of genomic aberrations
2009-12-16 | GSE19459 | GEO