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Links from GEO DataSets

Items: 9

1.

Investigation of the anti-tumor mechanism of tirabrutinib, a highly selective Bruton’s tyrosine kinase inhibitor, by transcriptomics

(Submitter supplied) Tirabrutinib is a highly selective BTK inhibitor for treating hematological malignancies. This study analyzed the anti-tumor mechanism of tirabrutinib with microarray analysis of ABC-DLBCL xenograft model tumors. The comprehensive gene expression analysis revealed that tirabrutinib downregulated IRF-4, MYC, and mTORC1 pathway-related genes in TMD8, suggesting the crucial roles of these pathways in ABC-DLBCL.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL14550
25 Samples
Download data: TXT
Series
Accession:
GSE210284
ID:
200210284
2.

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
3.

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
4.

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
5.

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
6.

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
7.

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
8.

Inhibitors of Bcl-2 and Bruton’s tyrosine kinase synergize to abrogate diffuse large B-cell lymphoma (DLBCL) growth

(Submitter supplied) Methods: DLBCL cell lines RIVA, U-2932 and OCI-LY3 were treated in vitro with ibrutinib (Ibru) or dimethyl sulfoxide (DMSO). Additionally, RIVA and U-2932 were orthotopically transplanted into MISTRG mice and mice were treated for two weeks with Ibru or vehicle. Tumor cells were isolated from the bone marrow at the study endpoint. The total RNA was isolated and the mRNA profiles were generated by next-generation sequencing using the Illumina TruSeq mRNA stranded protocol. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
30 Samples
Download data: TXT
9.

Effect of clinically observed BTK mutations on gene expression during cell proliferation and differentiation in TMD8 cells

(Submitter supplied) To investagate the clinically observed BTK C481S, C481F, C481Y and C481R mutations in the regulation of B cell receptor signaling, we extablished TMD8 cells expressing BTK C481S, C481F, C481Y and C481R in which endogenous BTK was inactivated by ibrutinib. We then performed gene expression profiling analysis using data obtained from RNA-seq of 20 different cells after DMSO or 10 nM ibrutinib treatment from two indenpendent experiments.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
20 Samples
Download data: TXT
Series
Accession:
GSE207322
ID:
200207322
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