Project description:RNA-Seq profiling of Burkitt Lymphoma cell line (BL2) with B-cell activating factor (BAFF) for 24 hrs . The Burkitt Lymphoma cell line were either only cultured in cell culture medium supplemented with 10 mM HEPES at 1 × 106 cells/ml or additionally incubated with B-cell activating factor (BAFF) for 24 hrs
Project description:Microarray profiling of Burkitt Lymphoma cell line (BL2) with B-cell activating factor (BAFF) for 24 hrs . The Burkitt Lymphoma cell line were either only cultured in cell culture medium supplemented with 10 mM HEPES at 1 × 106 cells/ml or additionally incubated with B-cell activating factor (BAFF) for 24 hrs
Project description:The purpose of the study was to identify downstream gene targets regulated by a new alternative splice of BAFF (B-Cell Activating factor belonging to the TNF Family) that we called Delta4-BAFF (because it characterized by an alternative splice of exon 4). To do this we used human burkitt's lymphoma cell line (RAMOS) stably transfected with Delta4-BAFF or stably transfected with Delta4-BAFF mutated on its N-glycosylation site (Delta4-BAFF-N124D). One control was used : RAMOS stably transfected with empty vector (pIRES2-GFP from Clontech)
Project description:The distinction between the Burkitt lymphoma and diffuse large B-cell lymphoma is imprecise using current diagnostic criteria. We applied transcriptional and genomic profiling to molecularly define Burkitt lymphoma. Gene expression profiling employing Affymetrix GeneChips (U133A) was performed in 220 mature aggressive B-cell lymphomas, including a core group of eight Burkitt lymphomas, which fulfilled all diagnostic criteria of the WHO classification. A molecular signature of Burkitt lymphoma was generated. Chromosomal abnormalities were detected by interphase fluorescence in-situ hybridization and array comparative genomic hybridization. The molecular Burkitt lymphoma signature identified 44 cases. Fifteen of these cases lacked a morphology typical for Burkitt/Burkitt-like lymphoma. The vast majority (88%) of the 176 lymphomas without the molecular Burkitt lymphoma signature represented diffuse large B-cell lymphomas. In 20% of these cases a MYC break was detectable which was associated with complex chromosomal changes. Our molecular definition of Burkitt lymphoma sharpens and extends the spectrum of Burkitt lymphoma. In mature aggressive B-cell lymphomas without a Burkitt lymphoma signature, a chromosomal break in the MYC locus proved to be associated with adverse clinical outcome. Keywords: Gene expression
Project description:The distinction between the Burkitt lymphoma and diffuse large B-cell lymphoma is imprecise using current diagnostic criteria. We applied transcriptional and genomic profiling to molecularly define Burkitt lymphoma. Gene expression profiling employing Affymetrix GeneChips (U133A) was performed in 220 mature aggressive B-cell lymphomas, including a core group of eight Burkitt lymphomas, which fulfilled all diagnostic criteria of the WHO classification. A molecular signature of Burkitt lymphoma was generated. Chromosomal abnormalities were detected by interphase fluorescence in-situ hybridization and array comparative genomic hybridization. The molecular Burkitt lymphoma signature identified 44 cases. Fifteen of these cases lacked a morphology typical for Burkitt/Burkitt-like lymphoma. The vast majority (88%) of the 176 lymphomas without the molecular Burkitt lymphoma signature represented diffuse large B-cell lymphomas. In 20% of these cases a MYC break was detectable which was associated with complex chromosomal changes. Our molecular definition of Burkitt lymphoma sharpens and extends the spectrum of Burkitt lymphoma. In mature aggressive B-cell lymphomas without a Burkitt lymphoma signature, a chromosomal break in the MYC locus proved to be associated with adverse clinical outcome. Experiment Overall Design: 220 diffuse large B-cell lymphoma and Burkitt lymphoma samples hybridized to 221 HGU133A Affymetrix GeneChips
Project description:Tumor necrosis factor-associated factors 2 and 3 (TRAF2 and TRAF3) were shown to function in a co-operative and non-redundant manner to suppress nuclear factor-κB2 (NF-κB2) activation, gene expression and survival in mature B cells. In the absence of this suppressive activity, B cells developed independently of the obligatory B cell survival factor, BAFF (B cell activating factor of the tumor necrosis factor family). This constitutive, lineage-specific suppression of B cell survival by TRAF2 and TRAF3 determines the requirement for BAFF to sustain B cell development in vivo. We wished to investigate the effect on gene expression in B cells which lacked the negative regulators TRAF2 and TRAF3, and hence had hyperactive NF-kB2 signalling. As Baff-tg mice display a similar phenotype, and have a genetic modification which acts in the same pathway, yet further up, than TRAF2 and TRAF3, we wished to compare and contrast Baff-tg B cells with TRAF2 and TRAF3 deficient B cells. This analysis should identify genes that are important in B cell survival. Experiment Overall Design: Lymph node B cells were purified from Traf2 B cell knockout mice, Traf3 B cell knockout mice, Baff-tg mice and respective controls. RNA was extracted and hybridised to Affymetrix 430 2.0 Mouse Genome Arrays. Samples were processed and hence analysed on three spearate days. Day 1 two control mice: Traf2lox/lox pool and CD19-cretg were compared to two knockout mice: Traf2DB 80 and Traf3DB 94. On Day 2 three control mice: Traf2lox/lox 77, Traf2lox/lox 79 and Traf3lox/lox 97 were compared to two knockout mice: Traf2DB 76 and Traf3DB 01. On Day 3 three control mice: WT33, WT34, WT35 were compared to three Baff-tg mice: Baff-tg 99, Baff-tg 100, Baff-tg 101.