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Links from GEO DataSets

Items: 15

1.
Full record GDS5826

Multiple myeloma cell lines with acquired resistance to chemotherapeutic agent carfilzomib

Analysis of proteasome inhibitor carfilzomib-resistant multiple myeloma (MM) cell lines KMS-11/Cfz and KMS-34/Cfz, after 1 week of growth in the absence of carfilzomib. Results provide insight into the molecular mechanisms underlying the acquisition of proteasome inhibitor resistance in MM.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 4 cell line, 2 cell type sets
Platform:
GPL570
Series:
GSE69078
12 Samples
Download data: CEL
2.

Comparison of the gene expression profiles of carfilzomib-resistant derivatives versus parental human myeloma cell lines

(Submitter supplied) KMS-11 and KMS-34 cells were exposed to stepwise increasing concentrations of carfilzomib over a period of 18 weeks: cells adapted to growth in 4 nM carfilzomib by 4 weeks, in 6 nM in another 6 weeks and in 12 nM after a further 8 weeks. The resulting cell cultures, denoted KMS-11/Cfz and KMS-34/Cfz, respectively, retained resistance to carfilzomib even when tested after removal of selective pressure for approximately 8 weeks.
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5826
Platform:
GPL570
12 Samples
Download data: CEL
Series
Accession:
GSE69078
ID:
200069078
3.

Comparative expression analysis of carfilzomib-resistant and parental LP-1 human multiple myeloma cells

(Submitter supplied) LP-1 cells were exposed to stepwise increasing concentrations of carfilzomib over a period of 18 weeks: cells adapted to growth in 4 nM carfilzomib by 4 weeks, in 6 nM in another 6 weeks and in 12 nM after a further 8 weeks. The resulting cell culture, denoted LP-1/Cfz, retained resistance to carfilzomib even when tested after removal of selective pressure for approximately 8 weeks.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
6 Samples
Download data: CEL
Series
Accession:
GSE78069
ID:
200078069
4.

Targeting steroid receptor co-activator 3 sensitizes myeloma cell to proteasome inhibitor treatment through NSD2-mediated phase separation and chromatin remodeling

(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:
GPL20795 GPL23227
14 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE156872
ID:
200156872
5.

Targeting steroid receptor co-activator 3 sensitizes myeloma cell to proteasome inhibitor treatment through NSD2-mediated phase separation and chromatin remodeling [RNA-Seq]

(Submitter supplied) Functional crosstalk between histone modifications and chromatin remodeling has emerged as a key regulatory mode of transcriptional control during cell fate decisions, but the underlying mechanisms are not fully understood. Here we demonstrate that some drug resistant genes were activated during myeloma resistant to bortezomib. Mechanistically, NSD2 can interact with SRC-3, its SET domain is responsible to H3K36me2 to enhance the transcriptional activity of SRC-3 target gene. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23227
8 Samples
Download data: TXT
Series
Accession:
GSE156871
ID:
200156871
6.

Targeting steroid receptor co-activator 3 sensitizes myeloma cell to proteasome inhibitor treatment through NSD2-mediated phase separation and chromatin remodeling [ChIP-Seq]

(Submitter supplied) Functional crosstalk between histone modifications and chromatin remodeling has emerged as a key regulatory mode of transcriptional control during cell fate decisions, but the underlying mechanisms are not fully understood. Here we demonstrate that NSD2/SRC-3 complex coordinates histone H3 lysine 36 dimethylation (H3K36me2) and transcriptional elongation factor Pol II to regulate chromatin dynamic and gene transcription during myeloma resistant to bortezomib. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20795
6 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE156870
ID:
200156870
7.

Control of Autophagic Cell Death by Caspase-10 in Multiple Myeloma

(Submitter supplied) We performed a loss-of-function, RNA interference screen to define new therapeutic targets in multiple myeloma, a genetically diverse plasma cell malignancy. Unexpectedly, we discovered that all myeloma lines require caspase-10 for survival, irrespective of their genetic abnormalities. The transcription factor IRF4 induces both caspase-10 and its associated protein cFLIPL in myeloma, generating a protease that does not induce apoptosis but rather blocks an autophagy-dependent cell death pathway. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL3278
40 Samples
Download data: GPR
Series
Accession:
GSE43878
ID:
200043878
8.

The role of FAM46C in myeloma cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Expression profiling by array
Platforms:
GPL11154 GPL17586
11 Samples
Download data: CEL, CHP
Series
Accession:
GSE99358
ID:
200099358
9.

The role of FAM46C in myeloma cells [array]

(Submitter supplied) FAM46C is one of the most recurrently mutated genes in multiple myeloma (MM), however its role in disease pathogenesis is not determined. Here we demonstrate that wild type (WT) FAM46C overexpression induces substantial cytotoxicity in MM cells. In contrast, FAM46C mutations found in MM patients abrogate this cytotoxicity indicating a MM survival advantage conferred by the FAM46C mutant phenotype. WT FAM46C overexpression downregulated IRF4, CEBPB, MYC and upregulated immunoglobulin (Ig) light chain and HSPA5/BIP. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17586
3 Samples
Download data: CEL, CHP
Series
Accession:
GSE99357
ID:
200099357
10.

The role of FAM46C in myeloma cells [sequencing]

(Submitter supplied) FAM46C is one of the most recurrently mutated genes in multiple myeloma (MM), however its role in disease pathogenesis is not determined. Here we demonstrate that wild type (WT) FAM46C overexpression induces substantial cytotoxicity in MM cells. In contrast, FAM46C mutations found in MM patients abrogate this cytotoxicity indicating a MM survival advantage conferred by the FAM46C mutant phenotype. WT FAM46C overexpression downregulated IRF4, CEBPB, MYC and upregulated immunoglobulin (Ig) light chain and HSPA5/BIP. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: TXT
Series
Accession:
GSE99356
ID:
200099356
11.

The mitochondrial protease LonP1 promotes proteasome inhibitor resistance in multiple myeloma.

(Submitter supplied) Purpose: We report the NGS-derived transcriptome profiling (paired-end RNA-seq) following proteasome inhibition in the multiple myeloma cell line MM.1S. Methods: MM.1S cells were treated for six hours with the synthetic proteasome inhibitor lactacystin or clinically-approved proteasome inhibitor bortezomib and RNA expression changes were quantified and compared to DMSO control-treated cells by RNA-sequencing.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
4 Samples
Download data: XLSX
Series
Accession:
GSE166122
ID:
200166122
12.

Super-enhancer profiling combined with CDK7 inhibition-transcripts identifies novel oncogenes of multiple myeloma.

(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
Platform:
GPL20301
48 Samples
Download data: BROADPEAK
Series
Accession:
GSE145938
ID:
200145938
13.

H3K27ac ChIP-seq for primary multiple myeloma patients’ samples (MM1-MM10)

(Submitter supplied) ChIP-seq analysis was performed in primary Multiple Myeloma patients’ samples to analyze acetylation of histone H3K27ac.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
20 Samples
Download data: BROADPEAK
Series
Accession:
GSE145891
ID:
200145891
14.

H3K27ac ChIP-seq for multiple myeloma cell lines, B-lymphoma cells and normal plasma cell

(Submitter supplied) ChIP-seq analysis was performed in Multiple Myeloma cell lines to analyze acetylation of histone H3K27ac.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
20 Samples
Download data: BROADPEAK
Series
Accession:
GSE145890
ID:
200145890
15.

RNA-seq analysis after THZ1 treatment in JJN3 and H929

(Submitter supplied) RNA-seq analysis was performed in JJN3 and H929 to analyze gene expression changes after THZ1 treatment.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
8 Samples
Download data: TXT
Series
Accession:
GSE145889
ID:
200145889
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