Germinal center (CD19+Fas+GL7+) and naive (CD19+Fas-GL7-) B cells were sorted from Peyer''s patches of littermate 12 weeks old WT C57BL/6 mice. Three biological replicates were analyzed, each composed of a pool of 5 female mice. RNA was purified from pellets of 2-2.5x10^4 cells and sequencing libraries were prepared from 100ng of total RNA per replicate. Overall design: Transcriptional profiling of germinal center and naive B cells from Peyer's patches of WT mice.
A broad atlas of somatic hypermutation allows prediction of activation-induced deaminase targets.
Sex, Age, Specimen part, Cell line, Subject
View SamplesMechanisms of immune regulation may control proliferation of aberrant plasma cells (PCs) in patients with the asymptomatic monoclonal gammopathy of undetermined significance (MGUS) preventing progression to active multiple myeloma (MM). We investigated the role of CD85j (LILRB1), an inhibitory immune checkpoint for B cell function, in MM pathogenesis.
Loss of the Immune Checkpoint CD85j/LILRB1 on Malignant Plasma Cells Contributes to Immune Escape in Multiple Myeloma.
Specimen part, Cell line
View SamplesAcadesine is a nucleoside analogue with known antileukemic effects in different neoplasms. We investigated the activity of acadesine ne exerts a cytotoxic effect in MCL and synergizes with rituximab supporting clinical examination of this strategy for MCL patients
Synergistic anti-tumor activity of acadesine (AICAR) in combination with the anti-CD20 monoclonal antibody rituximab in in vivo and in vitro models of mantle cell lymphoma.
Cell line, Treatment
View SamplesMultiple myeloma (MM) cells were treated with the BET inhibitor CPI203 alone and in combination with lenalidomide plus dexamethasone in vitro and in vivo (mouse xenograft).
The BET bromodomain inhibitor CPI203 improves lenalidomide and dexamethasone activity in <i>in vitro</i> and <i>in vivo</i> models of multiple myeloma by blockade of Ikaros and MYC signaling.
Specimen part, Cell line, Treatment
View SamplesPhosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway activation contributes to mantle cell lymphoma (MCL) pathogenesis and drug resistance. However, the use of mTOR inhibitors as single agents have shown limited clinical efficacy in relation with drug activation of feedback loops. Selective PI3K inhibition or dual PI3K/mTOR catalytic inhibition are different therapeutic approaches developed to achieve effective pathway blockage. Here, we evaluated the antitumor activity of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in primary MCL cells. We found that dual PI3K/mTOR inhibitor modulated angiogenesis, tumor invasiveness and cytokine signaling compared to a mTOR inhibitor and a pan-PI3K inhibitor in MCL.
Dual PI3K/mTOR inhibition is required to effectively impair microenvironment survival signals in mantle cell lymphoma.
Specimen part, Disease, Disease stage, Treatment
View SamplesCombination of GSI with fludarabine has a synergistic antileukemic effect in primary NOTCH1-mutated CLL cells
The γ-secretase inhibitor PF-03084014 combined with fludarabine antagonizes migration, invasion and angiogenesis in NOTCH1-mutated CLL cells.
Specimen part
View SamplesCells from 2 FL patients and 1 FL cell line were cultured for up to 48h, with no stroma or on top of HK cells pre-establised layers. RNA from FL cells was isolated after 24 and 48h of culture
Disruption of follicular dendritic cells-follicular lymphoma cross-talk by the pan-PI3K inhibitor BKM120 (Buparlisib).
Cell line, Time
View SamplesDouble Hit Lymphoma (DHL) were treated with the BRD4 inhibitor 100 nM CPI203 for 6h
The BET bromodomain inhibitor CPI203 overcomes resistance to ABT-199 (venetoclax) by downregulation of BFL-1/A1 in in vitro and in vivo models of MYC+/BCL2+ double hit lymphoma.
Specimen part, Cell line, Subject
View SamplesRole of CTCF in activated B cells. Overall design: Transcriptome profiling of CTCF deficient and proficient activated in vitro B cells.
CTCF orchestrates the germinal centre transcriptional program and prevents premature plasma cell differentiation.
Specimen part, Subject
View SamplesThe neural transcription factor SOX11 is overexpressed in aggressive lymphoid neoplasms mainly in mantle cell lymphoma (MCL), but its functional role in malignant B-cells is unknown. To identify target genes transcriptionally regulated by SOX11 in malignant lymphoid cells, we have used Gene Expression Profiling (GEP) after SOX11 silencing in MCL cell lines.
SOX11 regulates PAX5 expression and blocks terminal B-cell differentiation in aggressive mantle cell lymphoma.
Specimen part, Cell line
View Samples