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Links from GEO DataSets

Items: 20

1.

Gene expression data of parental and ibrutinib-resistant TMD8 cells.

(Submitter supplied) Diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL) are the most prevalent B-lymphocyte neoplasms in which abnormal activation of the Bruton’s tyrosine kinase (BTK)–mediated B-cell receptor (BCR) signaling pathway contributes to pathogenesis. Ibrutinib is an oral covalent BTK inhibitor that has shown some efficacy in both indications. To improve ibrutinib efficacy through combination therapy, we first investigated differential gene expression in parental and ibrutinib-resistant cell lines to better understand the mechanisms of resistance. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17586
4 Samples
Download data: CEL
Series
Accession:
GSE93985
ID:
200093985
2.

Expression data from DLBCL tumor biopsies and TMD8 cell line

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL570 GPL17586
92 Samples
Download data: CEL
Series
Accession:
GSE93986
ID:
200093986
3.

Expression data from DLBCL tumor biopsies

(Submitter supplied) Diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL) are the most prevalent B-lymphocyte neoplasms in which abnormal activation of the Bruton’s tyrosine kinase (BTK)–mediated B-cell receptor (BCR) signaling pathway contributes to pathogenesis. Ibrutinib is an oral covalent BTK inhibitor that has shown some efficacy in both indications. To improve ibrutinib efficacy through combination therapy, we first investigated differential gene expression in parental and ibrutinib-resistant cell lines to better understand the mechanisms of resistance. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
88 Samples
Download data: CEL
Series
Accession:
GSE93984
ID:
200093984
4.

Diffuse Large B Cell Lymphoma cell line with Acquired Resistance to PI3Kδ Inhibitor Idelalisib

(Submitter supplied) RNAseq profile of TMD8 cell lines resistant to Idelalisib treatment. Idelalisib resistant TMD8 cells were generated by continuous passage in the presence of 1 μM idelalisib for 8 weeks until stable resistance to idelalisib was established. Parallel cultures were grown in the presence of 0.1% DMSO as passage-matched, drug-sensitive control lines. Sensitive and resistant TMD8 cells were clonally isolated through two rounds of single cell limiting dilution
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
11 Samples
Download data: TXT
Series
Accession:
GSE93156
ID:
200093156
5.

Sensitivity to PI3K and AKT inhibitors is mediated by divergent molecular mechanisms in subtypes of diffuse large B-cell lymphoma

(Submitter supplied) Activated B-cell-like (ABC) and germinal center B-cell-like (GCB) diffuse large B-cell lymphoma (DLBCL) represent the two major molecular DLBCL subtypes. They are characterized by differences in clinical course and by divergent addiction to oncogenic pathways. To determine activity of novel compounds in these two subtypes, we conducted an unbiased pharmacologic in vitro screen. The phosphatidylinositol-3-kinase (PI3K) alpha/delta (PI3Ka/d) inhibitor AZD8835 showed marked potency in ABC DLBCL models, whereas the protein kinase B (AKT) inhibitor AZD5363 induced apoptosis in PTEN-deficient DLBCLs. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
40 Samples
Download data: TXT
Series
Accession:
GSE92619
ID:
200092619
6.

Synergistic activity of BET protein antagonist-based combinations in Mantle Cell Lymphoma cells sensitive or resistant to ibrutinib

(Submitter supplied) To determine the global transcriptome changes in mantle cell lymphoma cells following treatment with the BET bromodomain antagonist, JQ1 Mantle Cell Lymphoma (MCL) cells exhibit increased B cell receptor and NFkB activities. The BET protein BRD4 is essential for the transcriptional activity of NFkB. Here, we demonstrate that treatment with the BET protein bromodomain antagonist (BA) JQ1 attenuates MYC and CDK4/6, inhibits the nuclear RelA levels and the expression of NFκB target genes including Bruton’s Tyrosine Kinase (BTK) in MCL cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
6 Samples
Download data: CEL
Series
Accession:
GSE70651
ID:
200070651
7.

Combination of the MEK inhibitor pimasertib with BTK or PI3K-delta inhibitors is active in pre-clinical models of aggressive lymphomas

(Submitter supplied) assess the efficacy of Pimasertib to characterize its mechanism of action
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
6 Samples
Download data: TXT
Series
Accession:
GSE76757
ID:
200076757
8.

FBXO10 deficiency and BTK activation upregulate BCL2 expression in mantle cell lymphoma

(Submitter supplied) Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to identify BTK targets by RNA-seq and high-throughput data analysis and verify these genes by quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods Methods: mino/z138 sc4/shbtk stable cell lines were generated with tet-on system vector, small hairpins were induced for 48 hours after doxycycline addition, mRNA was exacted and used for RNA sequencing. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: TXT
9.

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

(Submitter supplied) Double Hit Lymphoma (DHL) were treated with the BRD4 inhibitor 100 nM CPI203 for 6h We used microarrays to uncover the mechanisms underlying CPI203 activity in Double Hit Lymphoma (DHL)
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13667
10 Samples
Download data: CEL
Series
Accession:
GSE98905
ID:
200098905
10.

Gene expression profile analysis of PLS-123 in xenograft model.

(Submitter supplied) To exploit targets or signaling pathways affected by PLS-123 during anti-tumor process, gene expression profiling was carried out in OCI-Ly7 inoculated xenograft model.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16686
10 Samples
Download data: CEL
Series
Accession:
GSE65817
ID:
200065817
11.

Gene expression profile analysis of PLS-123 in OCI-Ly7 cells

(Submitter supplied) To exploit targets or signaling pathways affected by PLS-123 during anti-tumor process, gene expression profiling was carried out in representative OCI-Ly7 cells treated for 24 hours.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
12 Samples
Download data: CEL
Series
Accession:
GSE65816
ID:
200065816
12.

Efficacy of BET protein proteolysis targeted chimera-based combinations against novel patient-derived models of Richter Transformation-Diffuse Large B-Cell Lymphoma

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL20301 GPL18573
42 Samples
Download data: TDF
Series
Accession:
GSE154463
ID:
200154463
13.

Efficacy of BET protein proteolysis targeted chimera-based combinations against novel patient-derived models of Richter Transformation-Diffuse Large B-Cell Lymphoma [RNA-Seq]

(Submitter supplied) RichterTransformation (RT) develops in CLL as an aggressive, therapy resistant diffuse large B cell lymphoma (RT-DLBCL), commonly clonally related (CLR) to the antecedent CLL. Lack of available pre-clinical models has hampered development of novel therapies for RT-DLBCL. Here,we report the profiles of genetic alterations, active enhancers, gene-expressions and anti-lymphoma drug-sensitivity patterns of first-ever established, patient-derived xenograft models of RT-DLBCLs, including CLR and clonally unrelated (CLUR) to antecedent CLL. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
27 Samples
Download data: TXT
Series
Accession:
GSE154462
ID:
200154462
14.

Efficacy of BET protein proteolysis targeted chimera-based combinations against novel patient-derived models of Richter Transformation-Diffuse Large B-Cell Lymphoma [ChIP-Seq]

(Submitter supplied) RichterTransformation (RT) develops in CLL as an aggressive, therapy resistant diffuse large B cell lymphoma (RT-DLBCL), commonly clonally related (CLR) to the antecedent CLL. Lack of available pre-clinical models has hampered development of novel therapies for RT-DLBCL. Here,we report the profiles of genetic alterations, active enhancers, gene-expressions and anti-lymphoma drug-sensitivity patterns of first-ever established, patient-derived xenograft models of RT-DLBCLs, including CLR and clonally unrelated (CLUR) to antecedent CLL. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
9 Samples
Download data: TDF
Series
Accession:
GSE154457
ID:
200154457
15.

Efficacy of BET protein proteolysis targeted chimera-based combinations against novel patient-derived models of Richter Transformation-Diffuse Large B-Cell Lymphoma [ATAC-Seq]

(Submitter supplied) RichterTransformation (RT) develops in CLL as an aggressive, therapy resistant diffuse large B cell lymphoma (RT-DLBCL), commonly clonally related (CLR) to the antecedent CLL. Lack of available pre-clinical models has hampered development of novel therapies for RT-DLBCL. Here,we report the profiles of genetic alterations, active enhancers, gene-expressions and anti-lymphoma drug-sensitivity patterns of first-ever established, patient-derived xenograft models of RT-DLBCLs, including CLR and clonally unrelated (CLUR) to antecedent CLL. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: TDF
Series
Accession:
GSE154456
ID:
200154456
16.

Gene expression signatures for Ibrutinib resistance in Diffuse Large B-cell Lymphoma (ABC-DLBCL)

(Submitter supplied) To understand the acquired resistance mechanism in DLBCL the cell lines (OCI-Ly1, Oci-Ly10 and HBL-1) were treated with Ibrutinib over time to generate resistant clone.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13497
18 Samples
Download data: TXT
Series
Accession:
GSE138126
ID:
200138126
17.

Highly Potent and Selective Interleukin-1 Receptor-Associated Kinase 4 Inhibitors for the Treatment of Lymphoid Malignancies

(Submitter supplied) Pathologic activation of the Toll-like receptor (TLR) pathway underlies various human disorders such as autoimmune diseases, chronic inflammatory diseases and lymphoid malignancies. Current therapy of these diseases relies on immunosuppressive or chemotherapeutic agents, but more effective therapeutics tailored to disease-causing mechanisms are needed. Pivotal to TLR signaling is the IL-1 receptor-associated kinase 4 (IRAK4), which is recruited to TLRs by the adaptor protein MyD88. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4133
16 Samples
Download data: TXT
Series
Accession:
GSE63029
ID:
200063029
18.

Divergent Mechanisms of Oncogenic B Cell Receptor Signaling in Lymphoma

(Submitter supplied) B cell receptor (BCR) signaling has emerged as a therapeutic target in B cell lymphomas, but the precise deployment of inhibitors to target oncogenic BCR signaling requires detailed knowledge of the signaling cascades that the BCR triggers in individual tumors. Here, we have used CRISPR-Cas9 screens to investigate whether the ABC and GCB molecular subtypes of diffuse large B cell lymphoma (DLBCL) utilize distinct BCR signaling modes to sustain their proliferation and survival. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4133
8 Samples
Download data: TXT
Series
Accession:
GSE99276
ID:
200099276
19.

Exploiting Synthetic Lethality for the Therapy of ABC Diffuse Large B Cell Lymphoma

(Submitter supplied) Knowledge of essential oncogenic mutations can inspire therapeutic strategies that are synthetically lethal, affecting cancer cells bearing an oncogenic mutation while sparing normal cells. Lenalidomide is emerging as an active agent in diffuse large B cell lymphoma (DLBCL), especially for the activated B cell-like (ABC) subtype, but the mechanism of its action is unknown. Here we show that lenalidomide kills ABC DLBCL cells by augmenting the production of interferon 3/4, which these cells are predisposed to produce by their oncogenic MYD88 mutations. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4133
8 Samples
Download data: TXT
Series
Accession:
GSE33012
ID:
200033012
20.

Co-addiction to IRF4 and SPIB in ABC-DLBCL

(Submitter supplied) RNA interference screens identified the transcription factor IRF4 as essential for the survival of the activated B-cell-like subtype of diffuse large B-cell lymphoma (ABC-DLBCL). Analysis of IRF4 genomic targets in ABC-DLBCL and Multiple Myeloma (MM) revealed that IRF4 regulates distinct networks in these cancers. IRF4 peaks in ABC-DLBCL, but not MM, were enriched for a composite ETS-IRF DNA motif that can be bound by heterodimers of IRF4 and the ETS-family transcription factor SPIB, whose expression is also essential for ABC-DLBCL survival. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4133
32 Samples
Download data: TXT
Series
Accession:
GSE32456
ID:
200032456
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