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Links from GEO DataSets

Items: 20

1.

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
2.

Phosphatidylinositol 3-Kinase (PI3K) delta blockade increases genomic instability in B cells

(Submitter supplied) Activation-induced cytidine deaminase (AID) is a B-cell specific enzyme that targets immunoglobulin (Ig) genes to initiate class switch recombination (CSR) and somatic hypermutation (SHM). Through off-target activity, however, AID has a much broader impact on genomic instability by initiating oncogenic chromosomal translocations and mutations involved in lymphoma development and progression. AID expression is tightly regulated in B cells and its overexpression leads to enhanced genomic instability and lymphoma formation. more...
Organism:
Homo sapiens; Mus musculus
Type:
Other; Expression profiling by high throughput sequencing
Platforms:
GPL13112 GPL15520 GPL16417
162 Samples
Download data: BED, TXT
Series
Accession:
GSE77788
ID:
200077788
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.

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.

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
9.

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
10.

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
11.

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
12.

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
13.

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
14.

Genome-wide CRISPR screen of rituximab induced cell depletion

(Submitter supplied) We screened the genome of OCI-Ly-7, a Diffuse Large B-cell Lymphoma cell line, for genes mediating the response to rituximab treatment. We utilized the genome-wide library GeCKO v2 (A+B) from Feng Zhang. (Addgene#1000000049)
Organism:
Homo sapiens; unidentified plasmid
Type:
Other
Platforms:
GPL23227 GPL27656
5 Samples
Download data: TXT
Series
Accession:
GSE139385
ID:
200139385
15.

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
16.

EGR1-mediated ibrutinib resistance

(Submitter supplied) We established two representative ABC DLBCL cell lines (TMD8 and OCI-Ly10) with ibrutinib resistance by gradually increasing the concentration of ibrutinib during passage in culture. RNA-seq analysis demonstrated that the BCR pathway gene signature is enriched in resistant cell lines when compared to parental cells. The most upregulated gene is EGR1, a transcription factor that activates multiple oncogenic pathways including MYC and E2F. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
26 Samples
Download data: TXT, VCF
Series
Accession:
GSE223150
ID:
200223150
17.

Response to Bruton's tyrosine kinase inhibitors in aggressive lymphomas linked to chronic selective autophagy

(Submitter supplied) We uncovered an autophagic pathway regulating survival in ABC DLBCL upon BTK inhibition using genome wide CRISPR screening. To investigate the mechanism of action of this unique form of autophagy, we performed RNA-seq on TMD8 cells knocked out for various ATG genes that either showed resistance to BTK inhibitors (ATG9A, ATG101, ATG14, RB1CC1, WIPI2), those that did not (ATG5, ATG7, ULK1 and 2 DKO, or non-targetingcontrol), or TMD8 cells knocked out for the known NF-kB negative regulator TNFAIP3. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
44 Samples
Download data: TXT
Series
Accession:
GSE227465
ID:
200227465
18.

Effect of Idelalisib in follicular lymphoma monocultures and cocultured with follicular dendritic cells (FDC)

(Submitter supplied) Follicular Lymphoma primary cells (FL) were treated with the PI3K delta inhibitor idelalisib (500nM, 48h) in the presence or absence of follicular dendritic cells We used microarrays to uncover the mechanisms underlying mechanism of resistance and sensitivity of FL to idelalisib
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13667
20 Samples
Download data: CEL
Series
Accession:
GSE130918
ID:
200130918
19.

Gene expression data from biological replicates of imatinib and nilotinib resistant K-562 cells.

(Submitter supplied) Resistant cells were generated by stepwise exposure to increasing concentrations of imatinib or nilotinib to establish 0.5 and 2 µM imatinib and 0.05 µM nilotinib resistant cells. This procedure was performed twice independently to establish biological replicates of TKI resistance. We performed microarrays (Clariom S) to analyze the changes in gene expression during the development of TKI resistance.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL23159
28 Samples
Download data: CEL, CHP
Series
Accession:
GSE227347
ID:
200227347
20.

RNA sequencing reveals that withaferin A reduces overexpression of Bruton's tyrosine kinase in glucocorticoid resistant multiple myeloma cells

(Submitter supplied) Multiple myeloma (MM) is an incurable hematological malignancy characterized by the uncontrolled growth of plasma cells in the bone marrow. The major barrier in treating MM is the occurrence of primary and acquired therapy resistance to multiple existing anti-cancer drugs. Often, this therapy resistance is associated with constitutive activation of Bruton tyrosine kinase (BTK) dependent B-cell receptor (BCR) signaling. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23227
12 Samples
Download data: TXT
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