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accession-icon DRP001263
RNA-seq analysis of Fus-knocked down N2A cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To analyze role of FUS in RNA processing, RNA-seq analysis was performed using mouse neuroblastoma cell line, Nuero2A (N2A) cells. N2A cells were treated with Fus-siRNA or control siRNA.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE39865
The gene expression analysis of the spinal cord of SBMA (Spinal Bulbar Muscular Atrophy) model mice
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To identify the gene expression changes that are specific to SBMA, we prepared total mRNA samples from the spinal cords of transgenic mice carrying a full-length human AR with 97 CAGs (AR-97Q), transgenic mice bearing a wild-type allele of AR with 24 CAGs (AR-24Q), and the wild-type littermates of the AR-97Q mice (C57BL/6). We used AR-97Q (Line #7-8) male mice because they show progressive muscular atrophy and weakness as well as SBMA-like pathology such as the accumulation of the pathogenic androgen receptor in the nucleus of motor neurons.

Publication Title

Naratriptan mitigates CGRP1-associated motor neuron degeneration caused by an expanded polyglutamine repeat tract.

Sample Metadata Fields

Sex

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accession-icon GSE27583
mRNA decay analysis in the mouse myoblast cell line, C2C12 cells treated with conrtol-, Cugbp1- or Mbnl1-siRNA
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

CUGBP1 and MBNL1 are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. Using HITS-CLIP anlysis, we found CUGBP1 and MBNL1 preferentially bind to alternatively spliced introns and exons, as well as to the 3' UTRs.

Publication Title

CUGBP1 and MBNL1 preferentially bind to 3' UTRs and facilitate mRNA decay.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE103941
Expression data from mice liver drinking Hydrogen water
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Liver RNA samples from C57BL6 mice drinking Hydrogen water for 4 weeks

Publication Title

Molecular hydrogen upregulates heat shock response and collagen biosynthesis, and downregulates cell cycles: meta-analyses of gene expression profiles.

Sample Metadata Fields

Specimen part

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accession-icon GSE66604
Inhibition of ABCB1 Overcomes Cancer Stem Cell-like Properties and Acquired Resistance to MET inhibitor in Non-Small Cell Lung Cancer
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations have shown a dramatic response to EGFR inhibitors (EGFR-TKI). EGFR T790M mutation and MET amplification have been recognized as major mechanisms of acquired resistance to EGFR-TKI. Therefore, MET inhibitors have recently been used in NSCLC patients in clinical trials. In this study, we tried to identify the mechanism of acquired resistance to MET inhibitor. We analyzed the antitumor effects of two MET inhibitors, PHA-665752 and crizotinib, in 10 NSCLC cell lines. EBC1 cells with MET amplification were the only cells that were sensitive to both MET inhibitors. We established PHA-665752-resistant EBC1 cells, namely EBC1-R cells. EBC1-R cells showed overexpression of ATP-binding cassette sub-family B member 1 (ABCB1) as well as phosphorylation of MET. EBC1-R cells grew as cell spheres that exhibited cancer stem cell-like (CSC) properties and epithelial mesenchymal transition (EMT). The levels of two miRNAs, miR-374a and miR-138 which targeted ABCB1, were decreased in EBC1-R cells. ABCB1 siRNA and ABCB1 inhibitor elacridar could reduce sphere numbers and suppress EMT. Elacridar could also reverse the resistance to PHA-665752 in EBC1-R cells. Our study demonstrated that ABCB1 overexpression which was associated with CSC properties and EMT was involved in the acquired resistance to MET inhibitor. Inhibition of ABCB1 might be a novel therapeutic strategy for NSCLC patients with acquired resistance to MET inhibitor.

Publication Title

Inhibition of ABCB1 Overcomes Cancer Stem Cell-like Properties and Acquired Resistance to MET Inhibitors in Non-Small Cell Lung Cancer.

Sample Metadata Fields

Cell line

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accession-icon GSE95214
Ventral prostate in male F344 rats: Control vs. PhIP treatment
  • organism-icon Rattus norvegicus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

The gene expression profling between Control and 300 mg/kg PhIP treatment in ventral prostate lobe of male F344 rats

Publication Title

Early detection of prostate carcinogens by immunohistochemistry of HMGB2.

Sample Metadata Fields

Specimen part

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accession-icon DRP003593
Gene expression profiles of mouse spinal motor neurons
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Gene expression profiles of mouse spinal motor neurons are compared to those in cells in posterior horn region.

Publication Title

R-spondin 2 promotes acetylcholine receptor clustering at the neuromuscular junction via Lgr5.

Sample Metadata Fields

Cell line

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accession-icon DRP001120
Time course RNA-sequence of Ras-induced NIH 3T3 cells
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Genome-wide analysis of transcription at various times after expression of oncogenic Ras in mouse NIH 3T3 cells.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE32646
GSTP1 expression predicts poor pathological complete response to neoadjuvant chemotherapy in ER-negative breast cancer
  • organism-icon Homo sapiens
  • sample-icon 110 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The purpose of the present study was to investigate the association of glutathione S-transferase P1 (GSTP1) expression with resistance to neoadjuvant paclitaxel followed by 5-fluorouracil/epirubicin/cyclophosphamide (P-FEC) in human breast cancers. The relationship of GSTP1 expression and GSTP1 promoter hypermethylation with intrinsic subtypes was also investigated. In this study, primary breast cancer patients (n = 123, stage II-III) treated with neoadjuvant P-FEC were analyzed. Tumor samples were obtained by vacuum-assisted core biopsy before P-FEC. GSTP1 expression was determined using immunohistochemistry, GSTP1 promoter methylation index (MI) using bisulfite methylation assay and intrinsic subtypes using DNA microarray. The pathological complete response (pCR) rate was significantly higher in GSTP1-negative tumors (80.0%) than GSTP1-positive tumors (30.6%) (P = 0.009) among estrogen receptor (ER)-negative tumors but not among ER-positive tumors (P = 0.267). Multivariate analysis showed that GSTP1 was the only predictive factor for pCR (P = 0.013) among ER-negative tumors. Luminal A, luminal B and HER2-enriched tumors showed a significantly lower GSTP1 positivity than basal-like tumors (P = 0.002, P < 0.001 and P = 0.009, respectively), while luminal A, luminal B and HER2-enriched tumors showed a higher GSTP1 MI than basal-like tumors (P = 0.076, P < 0.001 and P < 0.001, respectively). In conclusion, these results suggest the possibility that GSTP1 expression can predict pathological response to P-FEC in ER-negative tumors but not in ER-positive tumors. Additionally, GSTP1 promoter hypermethylation might be implicated more importantly in the pathogenesis of luminal A, luminal B and HER2-enriched tumors than basal-like tumors.

Publication Title

GSTP1 expression predicts poor pathological complete response to neoadjuvant chemotherapy in ER-negative breast cancer.

Sample Metadata Fields

Age, Specimen part, Disease stage

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accession-icon GSE56026
Gene expression in human endometrial cancer tissues and serous papillary endometrial cancer cell line, SPAC-1L, treated by STAT1-siRNA and/or IFN-gamma
  • organism-icon Homo sapiens
  • sample-icon 71 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Endometrial cancer is one of the most common gynecologic malignancies, and patients with high grade disease, especially serous papillary subtype (SPEC) are often related to the poor outcomes. Recent genome-wide analyses have revealed that SPEC exhibits gene expression profiles that are distinct from the endometrioid histologic subtype; therefore, it is important to identify the SPEC driver genes or pathways responsible for the inherently aggressive phenotypes and to develop SPEC-specific therapies to target these driver genes or pathways.

Publication Title

STAT1 drives tumor progression in serous papillary endometrial cancer.

Sample Metadata Fields

Specimen part, Cell line

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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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Developed by the Childhood Cancer Data Lab

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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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