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accession-icon GSE64762
Expression Data from Gastrointestinal Stromal Tumor (GIST) Cell Lines
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Activating mutations in either KIT or PDGFRA are present in approximately 90% of gastrointestinal stromal tumors (GISTs). Although treatment with the KIT and PDGFR inhibitor imatinib can control advanced disease in about 80% of GIST patients, the beneficial effect is not durable. Here, we report that ligands from the FGF family reduced the effectiveness of imatinib in GIST cells, and FGF2 and FGFR1 are highly expressed in all primary GIST samples examined. The combination of KIT and FGFR inhibition showed increased growth inhibition in imatinib-sensitive GIST cell lines in the presence or absence of added FGF2 in vitro, and delayed tumor regrowth in vivo. In addition, inhibition of mitogen-activated protein kinase (MAPK) signaling by imatinib was not sustained in GIST cells. An extracellular signal-regulated kinase (ERK) rebound occurred through activation of FGF signaling, and was repressed by FGFR1 inhibition. Downregultation of Sprouty proteins played a role in the imatinib-induced feedback activation of FGF signaling in GIST cells.

Publication Title

FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors.

Sample Metadata Fields

Cell line

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accession-icon GSE67051
Gene expression analysis in EGFR-mutant NSCLC cells treated with erlotinib versus DMSO
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This experiment is designed to detect genes differentially expressed in 2uM erlotinib treatment versus DMSO treatment and to identify differential gene set enrichments.

Publication Title

Inhibition of Casein Kinase 1 Alpha Prevents Acquired Drug Resistance to Erlotinib in EGFR-Mutant Non-Small Cell Lung Cancer.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP056033
SF3B1 Degron knockdown RNA-seq
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Knockdown of mutant and/or wild-type SF3B1 in MEL202 cell line by Degron knock-in, followed by RNA-seq, to identify splicing events governed by mutant SF3B1. Overall design: Control: parental MEL202 cell line. Experiments: mutant-SF3B1 knockdown; wildtype-SF3B1 knockdown; mutant SF3B1 knockout. Treatments: each of these four conditions plus and minus shld.

Publication Title

A chemical genetics approach for the functional assessment of novel cancer genes.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP055023
Neonatal na誰ve CD8+ T cells have effector-like gene expression that prevents memory cell formation [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Neonates are intrinsically defective at creating memory CD8+ T cells in response to infection with intracellular pathogens. Here we investigated differential of small RNAs, transcription factors, and chemokine receptors regulation in neonates as compared to adults before and during infection. We found that prior to infection, na誰ve cells have a different expression profile for many microRNAs, and gene targets of these microRNAs show widespread expression differences. These targets and other changes in gene expression in na誰ve cells result in neonatal cells that get activated more easily, express chemokine receptors that home to sites of infection, and are less protected from apoptosis during contraction. As a result, changes in neonatal na誰ve cells drive effector cell terminal differentiation at the expense of creating long-lived memory cells. Overall design: total RNAs were sequenced from adult and neonatal CD8+ T cells before and during infection

Publication Title

MicroRNAs and Their Targets Are Differentially Regulated in Adult and Neonatal Mouse CD8+ T Cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP055022
Neonatal na誰ve CD8+ T cells have effector-like gene expression that prevents memory cell formation [3''UTR-seq]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Neonates are intrinsically defective at creating memory CD8+ T cells in response to infection with intracellular pathogens. Here we investigated differential of small RNAs, transcription factors, and chemokine receptors regulation in neonates as compared to adults before and during infection. We found that prior to infection, na誰ve cells have a different expression profile for many microRNAs, and gene targets of these microRNAs show widespread expression differences. These targets and other changes in gene expression in na誰ve cells result in neonatal cells that get activated more easily, express chemokine receptors that home to sites of infection, and are less protected from apoptosis during contraction. As a result, changes in neonatal na誰ve cells drive effector cell terminal differentiation at the expense of creating long-lived memory cells. Overall design: PolyA RNA was selected and sequenced from adult and neonatal CD8+ T cells before and during infection

Publication Title

MicroRNAs and Their Targets Are Differentially Regulated in Adult and Neonatal Mouse CD8+ T Cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE44927
Transcriptional responses of control and MDV3100 resistant lines to DMSO or MDV3100
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

LNCaP-derived MDV3100-resistant clones were treated with MDV3100 for 24h prior to collection

Publication Title

An F876L mutation in androgen receptor confers genetic and phenotypic resistance to MDV3100 (enzalutamide).

Sample Metadata Fields

Cell line

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accession-icon GSE44924
Testing rescue of AR signaling by ectopic expression of mutant AR allele in the presence of MDV-3100
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Genetically engineered LNCaPs overexpressing various AR alleles were treated with 0.1% DMSO or 10uM MDV3100 for 24h prior to collection

Publication Title

An F876L mutation in androgen receptor confers genetic and phenotypic resistance to MDV3100 (enzalutamide).

Sample Metadata Fields

Cell line

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accession-icon GSE44867
Identification of targets regulated by HSF1 in response to HSP90 inhibitors
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A375 cells with inducible knockdown HSF1 with and without HSP90 inhibitor treatment

Publication Title

Targeting HSF1 sensitizes cancer cells to HSP90 inhibition.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE65561
Expression data from MSC-treated monocytes
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Chronic inflammation leading to pro-inflammatory macrophage infiltration contributes to the pathogenesis of type 2 diabetes and subsequently the development of diabetic nephropathy. Mesenchymal stem cells (MSCs) possess unique immunomodulatory and cytoprotective properties making them an ideal candidate for therapeutic intervention

Publication Title

Human mesenchymal stem cells alter the gene profile of monocytes from patients with Type 2 diabetes and end-stage renal disease.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE37605
Expression Data of Treg and Tconv Cells from FoxP3-GFP Chimeric and FoxP3-ires-GFP B6 and NOD Mice
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The aim of this study was to quantify the impact of chimeric Foxp3-GFP protein on the Treg cell transcriptional program.

Publication Title

An N-terminal mutation of the Foxp3 transcription factor alleviates arthritis but exacerbates diabetes.

Sample Metadata Fields

Sex, Age, Specimen part

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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