DLBCL patients
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA613053 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
Project description:Genomic profiles of DLBCL (Diffuse Large B-cell Lymphoma) patients 20 DLBCL patients were selected for detection of genomic aberrations Patient's DNA were hybridized against Promega control on Agilent G4410B arrays and scanned with the Agilent G2505B scanner.
2010-05-17 | E-GEOD-19459 | biostudies-arrayexpress
Project description:RNA extracted from diagnostic tumor samples of 52 patients affected by DLBCL was analyzed on the nCounter system using the PanCancer Immune Profiling Panel.
2021-07-13 | GSE147115 | 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: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:This study performed an in-depth investigation of the immune-molecular profiles of an unique cohort of extranodal diffuse large B-cell lymphoma (DLBCL) of the bone, with single primary bone (PB-)DLBCL and multiple localizations (polyostotic-DLBCL). A similar DLBCL cohort with nodal localizations only and germinal center B-cell (GCB) phenotype (nodal-DLBCL-GCB) was used as comparator. With comprehensive genomic mutational and gene gene-expression profiling (GEP), in total 103 DLBCLS were analyzed. Both molecular techniques revealed a shared mutational genomic and gene-expression transcriptomic profile for PB-DLBCL (n=51) and polyostotic-DLBCL (n=18), justifying a collective analysis as bone-DLBCL. Differential incidences of EZH2, IRF8, and HIST1H1E, and MYC mutations/rearrangements (p<0.05) confirmed the distinct oncogenic evolution of bone-DLBCL and nodal-DLBCL-GCB (n=34). Bone-DLBCL primarily exhibited an intermediate/rich immune TME GEP signature (p≤<0.005), based on published gene sets. Further unsupervised clustering identified two distinct groups, establishing a notable ‘immune-rich’ cluster dominated by bone-DLBCL (754%, p=0.0062). This immune-rich cluster demonstrated superior survival (p=≤0.0263) compared to the ‘immune-low’ cluster, which consisted mostly of nodal-DLBCL-GCB cases (61%). Gene-set enrichment analysis illustrated variations in cell proliferation and immune systemreceptor pathways for the immune-rich cluster (p<0.001), indicating a crucial role for the tumor microenvironment (TME) in disease behavior and outcome. Further supported by deconvolution applications (CIBERSORTx and single-sample gene-set enrichment analysis), The immune-rich cluster highlighted highlighting an abundantmainly regulatory T cells in immune-rich and cell proliferation in immune-low. infiltrate of NK/T, Treg, TFH and follicular dendritic cells (p<0.001). Conclusively, PB-DLBCL and polyostotic-DLBCL shared similar TME features and immune-molecular profiles. This study delineates tThe distinct immune-rich TME profile of bone-DLBCL, which is associated with a superior survival. These findings suggest that bone-DLBCL patients with immune-rich GEP might benefit from less intensive polychemotherapies and this could further shape targeted immunomodulatory strategies.
2025-04-22 | GSE273595 | GEO
Project description:The main purpose of the study was to identify biological prognostic factors that could be used to define poor risk diffuse large B-cell lymphoma (DLBCL) patients. We used exon array profiling to screen differentially expressed genes and splicing variants between clinically high risk patients, who have relapsed or remained in remission in response to dose dense chemoimmunotherapy. Study population consisted of 43 high-risk DLBCL/FL grade 3 patients less than 65 years old. The patients were treated in the Nordic phase II protocol with six courses of R-CHOEP14 followed by systemic central nervous system prophylaxis with one course of high dose methotrexate and one course of high dose cytarabine.
2012-03-30 | E-MEXP-3488 | 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 exon-based transcrition profiling with Affymetrix Human 1.0 ST Exon Array from pairwise tissue samples of 8 DLBCL/FL3B patients. Paired biopsies were taken at diagnosis and 1-2 days after the first cycle of chemoimmunotherapy (R-CHOP).
2015-01-14 | E-MTAB-2471 | biostudies-arrayexpress