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Expression data and Copy Number Variations from Diffuse Large B Cell Lymphoma (DLBCL) patients

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE136971 | GEO | 2019/09/05

REPOSITORIES: GEO

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Expression data and Copy Number Variations from Diffuse Large B Cell Lymphoma (DLBCL) patients

Project description:Expression data and Copy Number Variations from Diffuse Large B Cell Lymphoma (DLBCL) patients

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Copy Number Variations identified in 225 Diffuse Large B-Cell Lymphoma tumors

Project description:Copy Number Variations (CNVs) were identified performing Comparative Genomic Hybridization (CGH) on 225 patients after whole-genome amplification, using Agilent SurePrint G3 4x180K microarrays. CNVs were further integrated with gene expression (Affymetrix U133+2 arrays) and mutations (targeted DNA resequencing). Complete description of the methods, array quality checks and called segments are available as supplemental material in the corresponding publication.

2019-10-24 | GSE136962 | GEO

Paired copy number analysis of Diffuse Large B Cell Lymphoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-01-22 | GSE71394 | GEO

Expression data from Diffuse Large B Cell Lymphoma (DLBCL) patients

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

Paired copy number analysis of DLBCL Diffuse Large B Cell Lymphoma [SNP 6.0 Array]

Project description:Copy number analysis can be useful for assessing prognosis in diffuse large B cell lymphoma (DLBCL). We analyzed copy number data from tumor samples of 60 patients diagnosed with DLBCL de novo and their matched normal samples. We detected a total of 63 recurrent copy number alterations (CNAs), including 33 gains, 30 losses, and nine recurrent acquired copy number neutral loss of heterozygosity (CNN-LOH). Interestingly, 20% of cases acquired CNN-LOH of 6p21 locus, which involves the HLA region. In normal cells there were no CNAs but we observed CNN-LOH involving some key lymphoma regions such as 6p21 and 9p24.1 (5%) and 17p13.1 (2.5%) in DLBCL patients. Furthermore, a model with some specific CNA was able to predict the subtype of DLBCL, 1p36.32 and 10q23.31 losses being restricted to germinal center B cell-like (GCB) DLBCL. In contrast, 8p23.3 losses and 11q24.3 gains were strongly associated with the non-GCB subtype. A poor prognosis was associated with biallelic inactivation of TP53 or 18p11.32 losses, while prognosis was better in cases carrying 11q24.3 gains, which includes ETS1 and FLI1 genes. In summary, CNA abnormalities identify specific DLBCL groups, and we describe CN-LOH in germline cells from DLBCL patients that are associated with genes that probably play a key role in DLBCL development.

2016-01-22 | GSE71389 | GEO

Genome-wide characterization of copy number variations in diffuse large B-cell lymphoma with implications in targeted therapy.

Project description:Diffuse large B-cell lymphoma (DLBCL) is the aggressive form of haematological malignancies with relapse/refractory in ~ 40% of cases. It mostly develops due to accumulation of various genetic and epigenetic variations that contribute to its aggressiveness. Though large-scale structural alterations have been reported in DLBCL, their functional role in pathogenesis and as potential targets for therapy is not yet well understood. In this study we performed detection and analysis of copy number variations (CNVs) in 11 human DLBCL cell lines (4 activated B-cell-like [ABC] and 7 germinal-centre B-cell-like [GCB]), that serve as model systems for DLBCL cancer cell biology. Significant heterogeneity observed in CNV profiles of these cell lines and poor prognosis associated with ABC subtype indicates the importance of individualized screening for diagnostic and prognostic targets. Functional analysis of key cancer genes exhibiting copy alterations across the cell lines revealed activation/disruption of ten potentially targetable immuno-oncogenic pathways. Genome guided in silico therapy that putatively target these pathways is elucidated. Based on our analysis, five CNV-genes associated with worst survival prognosis are proposed as potential prognostic markers of DLBCL.

| S-EPMC8985800 | biostudies-literature

SOCS1 mutation subtypes predict divergent outcomes in diffuse large B-Cell lymphoma (DLBCL) patients.

Project description:Suppressor of cytokine signaling 1 (SOCS1) is frequently mutated in primary mediastinal and diffuse large B-cell lymphomas (DLBCL). Currently, the prognostic relevance of these mutations in DLBCL is unknown. To evaluate the value of the SOCS1 mutation status as a prognostic biomarker in DLBCL patients, we performed full-length SOCS1 sequencing in tumors of 154 comprehensively characterized DLBCL patients. We identified 90 SOCS1 mutations in 16% of lymphomas. With respect to molecular consequences of mutations, we defined two distinct subtypes: those with truncating (major) and those with non-truncating mutations (minor), respectively. The SOCS1 mutated subgroup or the minor/major subtypes cannot be predicted on clinical grounds; however, assignment of four established gene-expression profile-based classifiers revealed significant associations of SOCS1 major cases with germinal center and specific pathway activation pattern signatures. Above all, SOCS1 major cases have an excellent overall survival, even better than the GCB-like subgroup. SOCS1 minor cases had a dismal survival, even worse than the ABC gene signature group. The SOCS1 mutation subsets retained prognostic significance in uni- and multivariate analyses. Together our data indicate that assessment of the SOCS1 mutation status is a single gene prognostic biomarker in DLBCL.

| S-EPMC3702206 | biostudies-other

Integrated Copy Number Analysis of Epstein Barr Virus (EBV)-Positive Diffuse Large B-Cell Lymphoma (DLBCL)

Project description:Copy number analysis was performed on EBV+ DLBCL samples compared with EBV- DLBCL. We analyzed the genomic DNA from 18 cases of EBV+ DLBCL, 21 cases of EBV- DLBCL, and 13 cases of nonneoplastic tonsillar tissues using OncoScan FFPE Express 2.0 (MIP). No technical replication were done.

2014-02-01 | E-MTAB-1971 | biostudies-arrayexpress

Copy Number Variations identified in 225 Diffuse Large B-Cell Lymphoma tumors

Project description:Copy Number Variations identified in 225 Diffuse Large B-Cell Lymphoma tumors

| PRJNA564130 | ENA

Whole-Genome/Exome Sequencing Uncovers Mutations and Copy Number Variations in Primary Diffuse Large B-Cell Lymphoma of the Central Nervous System.

Project description:Background/objective: Identification of key genetic alterations is of importance in the targeted therapies of primary central nervous system lymphoma (PCNSL). However, only a small number of studies have been carried out in PCNSL. In this study, we further described the genetic mutations and copy number variations (CNVs) in PCNSL patients using whole-genome/exome sequencing (WGS/WES), as well as revealed their associations with patients' clinicopathological features and prognosis. Methods: Tumor specimens from 38 patients with primary diffuse large B-cell lymphoma of the central nervous system (CNS DLBCL) were enrolled to WGS (n = 24) or WES (n = 14). The CNVs and mutations of 24 samples (WGS) and 38 samples (WGS/WES) were characterized, respectively. The associations between CNVs and mutations with the overall survival rates of PCNSL patients were also evaluated. Results: The most common mutations were identified in IGLL5 (68%), PIM1 (63%), MYD88 (55%), CD79B (42%), BTG2 (39%), PCLO (39%), KMT2D (34%), and BTG1 (29%) genes. Among the mutated genes, EP300, ETV6, and HIST1H1E mutations were exclusively detected in the elderly, while DUSP2 mutations were associated with the immune microenvironment indicators. In addition, KMT2D mutation was associated with a poor prognosis. In addition, 488 CNVs including 91 gains and 397 deletions were observed across 24 samples from WGS results. Notably, 1q31.3 amplification was closely associated with the poor prognosis of PCNSL patients. Conclusion: This study further characterizes the genomic landscape of primary CNS DLBCL using WGS/WES, which provides insight into understanding the pathogenesis of PCNSL and fosters new ideas for the targeted treatment of PCNSL.

| S-EPMC9133733 | biostudies-literature

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