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Enhanced DNA repair and genomic stability identify a novel HIV related Diffuse Large B-cell Lymphoma subtype [aCGH]

ABSTRACT: Enhanced DNA repair and genomic stability identify a novel HIV related Diffuse Large B-cell Lymphoma subtype [aCGH]

PROVIDER: PRJNA489484 | ENA |

REPOSITORIES: ENA

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Enhanced DNA repair and genomic stability identify a novel HIV related Diffuse Large B-cell Lymphoma subtype [aCGH]

Project description:Transcriptional and genomic profiling study of HIV positive and HIV negative Diffuse Large B-Cell Lymphoma (DLBCL). Tumors were subtyped using the Lymph2Cx assay. Only GCB (germinal center like B-cell) subtypes were then subjected to digitial gene expression profiling and array comparative genomic hybridization (aCGH). The study used DNA extracted from FFPE DLBCL tumors derived from HIV(+) and HIV(-) patients to assess copy number variation differences between the HIV(+) and HIV(-) cohorts. aCGH data was correlated with gene expression & IHC data.

2019-06-03 | GSE119536 | GEO

Enhanced DNA repair and genomic stability identify a novel HIV related Diffuse Large B-cell Lymphoma subtype [nanostring]

Project description:Transcriptional and genomic profiling study of HIV positive and HIV negative Diffuse Large B-Cell Lymphoma (DLBCL). Tumors were subtyped using the Lymph2Cx assay. Only GCB (germinal center like B-cell) subtypes were then subjected to digitial gene expression profiling and array comparative genomic hybridization (aCGH). The study used total RNA extracted from FFPE DLBCL tumors derived from HIV(+) and HIV(-) patients to assess differential expression of known cancer genes. Gene expression was correlated with IHC and array CGH data.

2019-06-03 | GSE119534 | GEO

Enhanced DNA repair and genomic stability identify a novel HIV related Diffuse Large B-cell Lymphoma subtype

Project description:Enhanced DNA repair and genomic stability identify a novel HIV related Diffuse Large B-cell Lymphoma subtype

| PRJNA489482 | ENA

Enhanced DNA repair and genomic stability identify a novel HIV related Diffuse Large B-cell Lymphoma subtype [nanostring]

Project description:Enhanced DNA repair and genomic stability identify a novel HIV related Diffuse Large B-cell Lymphoma subtype [nanostring]

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Enhanced DNA repair and genomic stability identify a novel HIV related Diffuse Large B-cell Lymphoma subtype

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

2019-06-03 | GSE119537 | GEO

Genomic profiling of high-risk diffuse large B-cell lymphoma patients treated with dose-dense chemoimmunotherapy

Project description:The aim of the study was to identify molecular mechanisms involved in high risk diffuse large B-cell lymphomas (diffuse large B-cell lymphomas). <br>51 prospectively collected tumor samples from the patients treated in the Nordic phase II study with dose-dense chemoimmunotherapy followed by systemic CNS prophylaxis were analyzed by high resolution array comparative genomic hybridization (aCGH). <br>The aCGH data were combined with the transcriptomics information from the exon array and the data associated with survival.

2012-03-30 | E-MEXP-3463 | biostudies-arrayexpress

Gene expression profiling of HIV-associated diffuse large B-cell lymphomas from Malawi

Project description:To investigate the biological differences between HIV-, HIV+/ART-experienced and HIV+/ART-naive diffuse large B-cell lymphoma, we performed RNA sequencing of 70 pre-treatment formalin-fixed paraffin-embedded (FFPE) whole lymph node biopsies of diffuse large B-cell lymphoma.

2024-06-01 | GSE262621 | GEO

MCL1 is deregulated in subgroups of diffuse large B-cell lymphoma

Project description:MCL1 is an anti-apoptotic member of the BCL2 family that is deregulated in various solid and hematological malignancies. However, its role in the molecular pathogenesis of diffuse large B-cell lymphoma (DLBCL) is unclear. We analyzed gene expression profiling data from 350 DLBCL patient samples and detected that activated B-cell-like (ABC) DLBCLs express MCL1 at significantly higher levels compared to germinal center B-cell-like (GCB) DLBCL patient samples (p=2.7 x 10(-10)) [PMID 23257783]. Immunohistochemistry confirmed high MCL1 protein expression predominantly in ABC DLBCL in an independent patient cohort (n=249; p=0.001). To elucidate molecular mechanisms leading to aberrant MCL1 expression, we analyzed array comparative genomic hybridization (aCGH) data of 203 DLBCL samples [GSE11318] and identified recurrent chromosomal gains/amplifications of the MCL1 locus that occurred in 26% of ABC DLBCLs. In addition, aberrant STAT3 signaling contributed to high MCL1 expression in this subtype. Knockdown of MCL1 as well as treatment with the BH3-mimetic obatoclax induced apoptotic cell death in MCL1 positive DLBCL cell lines. In summary, MCL1 is deregulated in a significant fraction of ABC DLBCLs and contributes to therapy resistance. These data suggest that specific inhibition of MCL1 might be utilized therapeutically in a subset of DLBCLs. This GEO dataset is comprised of aCGH measurements for DLBCL cell lines, which are used in the above-mentioned paper. Cell lines were measured against the DNA of a healthy male donor who in turn was measured against a pool of healthy DNAs to correct for individual CNVs of the donor.

2013-01-04 | E-GEOD-43272 | biostudies-arrayexpress

PTEN loss deM-oM-,M-^Anes a PI3K/AKT pathway-dependent germinal center subtype of diffuse large B-cell lymphoma

Project description:Diffuse large B-cell lymphoma (DLBCL) represents a heterogeneous diagnostic category with distinct molecular subtypes that can be deM-oM-,M-^Aned by gene expression proM-oM-,M-^Aling. However, even within these deM-oM-,M-^Aned subtypes, heterogeneity prevails. To further elucidate the pathogenesis of these entities, we determined the expression of the tumor suppressor phosphatase and tensin homolog (PTEN) in 248 primary DLBCL patient samples. These analyses revealed that loss of PTEN was detectable in 55% of germinal center B-cell-like (GCB) DLBCLs, whereas this abnormality was found in only 14% of non-GCB DLBCL patient samples. In GCB DLBCL, the PTEN status was inversely correlated with activation of the oncogenic PI3K/ protein kinase B (AKT) pathway in both DLBCL cell lines and primary patient samples. Reexpression of PTEN induced cytotox- icity in PTEN-deM-oM-,M-^Acient GCB DLBCL cell line models by inhibiting PI3K/AKT signaling, indicating an addiction to this pathway in this subset of GCB DLBCLs. PI3K/AKT inhibition induced down-regulation of the transcription factor MYC. Reexpression of MYC rescued GCB DLBCL cells from PTEN-induced toxicity, identifying a regulatory mechanism of MYC expression in DLBCL. Finally, pharmacologic PI3K inhibition resulted in toxicity selectively in PTEN-deM-oM-,M-^Acient GCB DLBCL lines. Collectively, our results indicate that PTEN loss deM-oM-,M-^Anes a PI3K/ AKT-dependent GCB DLBCL subtype that is addicted to PI3K and MYC signaling and suggest that pharmacologic inhibition of PI3K might represent a promising therapeutic approach in these lymphomas. This GEO dataset is comprised of a) GEP measurements for 34 primary DLBCL patient samples plus two reference samples, b) 8 paired GEP measurements of the HT DLBCL cell line and c) aCGH measurements for two DLBCL cell lines in addition to previously published cell lines in GSE43272 (i.e., Sample GSM1059798). All of these data were used in the paper cited below.

2013-07-09 | E-GEOD-45495 | biostudies-arrayexpress

MCL1 is deregulated in subgroups of diffuse large B-cell lymphoma

2013-01-04 | GSE43272 | GEO