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Links from GEO DataSets

Items: 20

1.
Full record GDS5309

Sotrastaurin effect on mantle cell lymphoma cell lines

Analysis of various mantle cell lymphoma (MCL) lines treated with sotrastaurin (STN). Jeko-1 and Mino are STN-sensitive cell lines; Z-138 and Maver-1 are STN-insensitive cell lines. STN is a pan-protein kinase C (PKC) inhibitor. Results provide insight into the molecular response to PKC inhibition.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 agent, 4 cell line, 2 other sets
Platform:
GPL570
Series:
GSE42549
16 Samples
Download data: CEL
DataSet
Accession:
GDS5309
ID:
5309
2.

Transcriptional responses of mantle cell lymphoma (MCL) after NIK knockdown

(Submitter supplied) MCL lines were treated with or without 100ng/ml doxycycline for 7 days This experiment is designed to see if shRNA-mediated knockdown of NIK downregulates NFKB signaling in MCL lines with mutations in upstream regulators of the alternative pathway (TRAF2 & TRAF3)
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
12 Samples
Download data: CEL
Series
Accession:
GSE52435
ID:
200052435
3.

Transcriptional responses of mantle cell lymphoma (MCL) lines to IKKB inhibition

(Submitter supplied) MCL cell lines were treated with DMSO or 5uM AFN700 for 20hrs This experiment is designed to see if NFKB-target genes are downregulated by inhibition of IKKB in MCL cell lines that are insensitive to ibrutinib (BTK inhibitor) or sotrastaurin (PKC inhibitor)
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
16 Samples
Download data: CEL
Series
Accession:
GSE52434
ID:
200052434
4.

Transcriptional responses of mantle cell lymphoma (MCL) lines to PKC inhibition

(Submitter supplied) MCL lines (biological replicates) were treated with DMSO or 2.5uM Sotrastaurin for 3hrs This experiment is designed to see if a common set of genes is affected by Sotrastaurin (STN) treatment in STN-sensitive and STN-insensitive MCL lines.
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5309
Platform:
GPL570
16 Samples
Download data: CEL
Series
Accession:
GSE42549
ID:
200042549
5.

Mechanisms of constitutive NF-kappaB signaling in multiple myeloma

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL3278
12 Samples
Download data: GPR
Series
Accession:
GSE8487
ID:
200008487
6.

NFkB in multiple myeloma - EJM IkBa super-repressor

(Submitter supplied) Mechanisms of constitutive NF-kappaB signaling in multiple myeloma are unknown. An inhibitor of IkappaB kinase beta (IKKbeta), targeting the classical NF-kappaB pathway, was lethal to many myeloma cell lines. Several had elevated expression of NIK due to genomic alterations or enhanced protein stability while others had inactivating mutations or deletion of TRAF3. Both abnormalities triggered the classical and alternative NF-kappaB pathways. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL3278
4 Samples
Download data: GPR
Series
Accession:
GSE8477
ID:
200008477
7.

NFkB in multiple myeloma - L363 IKK inhibitor

(Submitter supplied) Mechanisms of constitutive NF-kappaB signaling in multiple myeloma are unknown. An inhibitor of IkappaB kinase beta (IKKbeta), targeting the classical NF-kappaB pathway, was lethal to many myeloma cell lines. Several had elevated expression of NIK due to genomic alterations or enhanced protein stability while others had inactivating mutations or deletion of TRAF3. Both abnormalities triggered the classical and alternative NF-kappaB pathways. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL3278
8 Samples
Download data: GPR
Series
Accession:
GSE8476
ID:
200008476
8.

Classical and/or alternative NF-kB pathway activation in multiple myeloma pathogenesis

(Submitter supplied) Mutations involving the NFKB pathway are present in at least 17% of multiple myeloma (MM) tumors and 40% of MM cell lines (MMCL). These mutations, which are thought to be progression events, enable MM tumors to become less dependent on extrinsic bone marrow signals that activate NFKB. Studies on a panel of 50 MMCL provide some clarification of the mechanisms through which these mutations act and the significance of classical vs alternative activation of NFKB. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
18 Samples
Download data: CEL
Series
Accession:
GSE18047
ID:
200018047
9.

Direct in vivo evidence for B-cell receptor and NF-KB activation in mantle cell lymphoma: role of the lymph node microenvironment and activating mutations. [RNA-Seq]

(Submitter supplied) We provide direct in vivo evidence for activation of the BCR and canonical NF-KB pathways in MCL that, in the absence of activating mutations, is dependent on the lymph node microenvironment. This finding provides a mechanistic explanation for the surprising efficacy of ibrutinib for the treatment of this type of lymphoma. Mutations in components of the BCR and NF-KB pathways are associated with cell-autonomous signaling and resistance to ibrutinib.
Organism:
Homo sapiens
Type:
Other
Platform:
GPL11154
16 Samples
Download data: TXT
Series
Accession:
GSE70926
ID:
200070926
10.

Direct in vivo evidence for B-cell receptor and NF-KB activation in mantle cell lymphoma: role of the lymph node microenvironment and activating mutations. [Affymetrix]

(Submitter supplied) We provide direct in vivo evidence for activation of the BCR and canonical NF-KB pathways in MCL that, in the absence of activating mutations, is dependent on the lymph node microenvironment. This finding provides a mechanistic explanation for the surprising efficacy of ibrutinib for the treatment of this type of lymphoma. Mutations in components of the BCR and NF-KB pathways are associated with cell-autonomous signaling and resistance to ibrutinib.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
55 Samples
Download data: CEL
Series
Accession:
GSE70910
ID:
200070910
11.

Targeting Non-proteolytic Protein Ubiquitination for the Treatment of Diffuse Large B Cell Lymphoma (Affy SNP6.0 Arrays)

(Submitter supplied) Chronic active B cell receptor (BCR) signaling, a hallmark of the ABC subtype of diffuse large B cell lymphoma (DLBCL), engages the CARD11-MALT1-BCL10 (CBM) adapter complex to activates IkappaB kinase (IKK) and the classical NF-kappaB pathway. Here we show that the CBM complex includes the E3 ubiquitin ligases cIAP1 and cIAP2, which are essential mediators of BCR-dependent NF-kappaB activity in ABC DLBCL. more...
Organism:
Homo sapiens
Type:
Genome variation profiling by SNP array
Platform:
GPL6801
5 Samples
Download data
Series
Accession:
GSE73639
ID:
200073639
12.

Targeting Non-proteolytic Protein Ubiquitination for the Treatment of Diffuse Large B Cell Lymphoma (Agilent Arrays)

(Submitter supplied) Chronic active B cell receptor (BCR) signaling, a hallmark of the ABC subtype of diffuse large B cell lymphoma (DLBCL), engages the CARD11-MALT1-BCL10 (CBM) adapter complex to activates IkappaB kinase (IKK) and the classical NF-kappaB pathway. Here we show that the CBM complex includes the E3 ubiquitin ligases cIAP1 and cIAP2, which are essential mediators of BCR-dependent NF-kappaB activity in ABC DLBCL. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL13607 GPL16699
20 Samples
Download data: TXT
Series
Accession:
GSE73281
ID:
200073281
13.

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
14.

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
15.

Gene expression profiling of human peripheral T cell lymphoma cases vs. reactive lymph nodes

(Submitter supplied) Peripheral T cell lymphoma (PTCL) is a very aggressive disease which currently lacks efficient targeted therapy. New therapeutic strategies are needed to improve the very poor outcome of these patients. However, little is known about the molecular pathogenesis of this disease. In this study, we performed a gene expression profiling analysis of a series of 38 PTCL cases in order to find deregulated pathways or genes that could become therapeutic agents for PTCL patients.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6480
44 Samples
Download data: TXT
Series
Accession:
GSE36172
ID:
200036172
16.

RNA-Seq for a differential gene expression bewteen KLHL14 wild-type(+/+) and KLHL14 knockout(-/-) TMD8 ABC-DLBCL cell line upon treatment with a BTK inhibitor, ibrutinib

(Submitter supplied) The goal of this study is to examine gene expression changes in TMD8 KLHL14(+/+) or TMD8 KLHL14(-/-) cells during ibrutinib treatment. The samples have 35 to 63 million pass filter reads with more than 92% of bases above the quality score of Q30.The average mapping rate of all samples is 95%. Unique alignment is above 86%. There are 3.65 to 6.25% unmapped reads.The mapping statistics are calculated using Picard software. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
8 Samples
Download data: TXT
17.

Oncogenic CARMA1 couples NF-κB and β-Catenin signaling in diffuse large B cell lymphomas

(Submitter supplied) Constitutive activation of the anti-apoptotic NF-κB signaling pathway is a hallmark of the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphomas (DLBCL) that is characterized by adverse survival. Recurrent oncogenic mutations are found in the scaffold protein CARMA1 (CARD11) that connects B-cell receptor (BCR) signaling to the canonical NF-κB pathway. We asked how far additional downstream processes are activated and contribute to the oncogenic potential of DLBCL-derived CARMA1 mutants. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
10 Samples
Download data: TXT
Series
Accession:
GSE70025
ID:
200070025
18.

Time course analysis of gene expression in BCR-stimulated splenic wild type and TAK1-/- B cell

(Submitter supplied) The activation signaling of transcription factor nuclear factor-kB (NF-kB) plays central role for immune system. One of key kinase mediating this pathway is TAK1 in adaptive and innate immunity. However, role of TAK1 in B cell receptor signaling is still unclear. To know effects of TAK1-deletion on the gene expression induced by anti-IgM, we performed the time course analysis in comparison of wild type with TAK1-deleted splenic B cells.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
20 Samples
Download data: CEL
Series
Accession:
GSE41176
ID:
200041176
19.

Critical role of PI3K signaling for NF-κB–dependent survival in a subset of activated B-cell–like diffuse large B-cell lymphoma cells

(Submitter supplied) The activated B-cell–like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL) represents a very aggressive human lymphoma entity. Constitutive NF-κB activation caused by chronic active B-cell receptor (BCR) signaling is common feature of many ABC DLBCL cells; however, the pathways linking BCR signaling to the NF-κB prosurvival network are largely unknown. Here we report that constitutive activity of PI3K and the downstream kinase PDK1 are essential for the viability of two ABC DLBCL cell lines that carry mutations in the BCR proximal signaling adaptor CD79B. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4133
12 Samples
Download data: TXT
Series
Accession:
GSE94610
ID:
200094610
20.

Compensatory IKKa activation of classical NF-kB signaling during IKKb inhibition

(Submitter supplied) A subtype of diffuse large B-cell lymphoma (DLBCL), termed activated B-cell-like (ABC) DLBCL, depends on constitutive NF-kB pathway signaling for survival. Small molecule inhibitors of IkB kinase b (IKKb), a key regulator of the NF-kB pathway, kill ABC DLBCL cells and hold promise for the treatment of this lymphoma type. We conducted an RNA interference genetic screen to investigate potential mechanisms of resistance of ABC DLBCL cells to IKKb inhibitors. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL3278
4 Samples
Download data: GPR
Series
Accession:
GSE11902
ID:
200011902
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