DLBCL gene expression
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ABSTRACT:
PROVIDER: EGAD00010001976 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Gene-expression profiling of a polyostotic-DLBCL and primary bone-DLBCL cohort compared to a nodal DLBCL GCB.
| PRJNA1142483 | ENA
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: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:Expression data from DLBCL expression study
| PRJNA669021 | ENA
Project description:Gene expression profiling was performed for 28 DLBCL primary clinical samples and assignment of activated B-cell-like(ABC)/germinal center B-cell-like (GCB) DLBCL classes, B-cell-associated gene signature (BAGS), and a probability of response to doxorubicin was performed for each sample.
2016-10-05 | GSE74266 | GEO
Project description:Microenvironment Cell Populations Affymetrix 133 Plus 2.0 series
| PRJNA341518 | ENA
Project description:Diffuse large B cell lymphoma (DLBCL) is the most common aggressive B cell lymphoma and accounts for nearly 40% of cases of B cell non-Hodgkin lymphoma. DLBCL is generally treated with R-CHOP chemotherapy, but many patients do not respond or relapse after treatment. Here, we analyzed the therapeutic potential of the tumor suppressor microRNA-28 (miR-28) for DLBCL, alone and in combination with the Bruton’s tyrosine kinase inhibitor ibrutinib. Combination therapy with miR-28 plus ibrutinib potentiated the anti-tumor effects of monotherapy with either agent by inducing a specific transcriptional cell-cycle arrest program that impairs DNA replication. The molecular actions of miR-28 and ibrutinib synergistically impair DNA replication by simultaneous inhibition of origin activation and fork progression. Moreover, we found that downregulation of the miR-28-plus-ibrutinib gene signature correlates with better survival of ABC-DLBCL patients. These results provide evidence for the effectiveness of a new miRNA-based ibrutinib combination therapy for DLBCL and unveil the miR-28-plus-ibrutinib gene signature as a new predictor of outcome in ABC-DLBCL patients.
2023-09-21 | GSE229786 | GEO
Project description:We studied 498 de-novo adult DLBCL cases, which had been diagnosed between January 2002 and October 2009, as part of the International DLBCL Rituximab-CHOP Consortium Program Study We perform global gene expression profiling from formalin fixed paraffin embedded 498 DLBCL tissues RNA by SPIA mediated microarray detection and identified the distinct subgroups of the disease within DLBCL, known as germinal-center-B-cell-like (GCB), activated B-cell-like (ABC), and unclassified DLBCL (UC). RNA of 498 FFPET DLBCL patient samples were extracted, amplified using a novel RNA amplicfication method, Single Primer Isothermal Amplification (SPIA, NuGen Inc.), and hybridized to Affymetrix HG-U133 Plus 2.0 GeneChips. This dataset is the collaboration between The University of Texas at MD Anderson Cancer Center and Roche Molecular Systems, Inc.
2012-07-31 | E-GEOD-31312 | biostudies-arrayexpress
Project description:human foreskin fibroblasts were infected with HCMV We monitor cellular gene expression network altered by HCMV entry using Affymetrix Human Genome U133 Plus 2.0 Array
2013-03-15 | GSE27974 | GEO