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accession-icon GSE54388
Identification of differentially expressed transcription factors in ovarian cancer
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Ovarian cancer is the fifth most common form of cancer in women in the United States. Epithelial ovarian cancer is the most common and is highly lethal. In 2014, there will be an estimated 21,980 new cases and 14,270 deaths from ovarian cancer in the United States. No major strides have been made to improve survival over the past decade. Ovarian cancer is notable for initial chemotherapy sensitivity (>75% response rates) using combination platinum and taxane chemotherapy following debulking surgery. However, eventually, the vast majority of these women (>75-80%) will have their cancer recur within 12 to 24 months after diagnosis and will die of progressively chemotherapy-resistant diseases. Transcription factors act as master switches of various biochemical pathways by regulating gene transcription. Large number of studies demonstrated the role of transcription factors in cancer development and progression. However, transcription factors involved in the pathogenesis of ovarian cancer have not been explored thoroughly. Therefore, we propose to using transcriptome profiling to generate a transcription factor gene signature for high-grade serous ovarian cancer.

Publication Title

ELF3 is a negative regulator of epithelial-mesenchymal transition in ovarian cancer cells.

Sample Metadata Fields

Specimen part, Disease

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accession-icon SRP149190
Transcriptional profile of monocytes in the colon in response to C. rodentium infection
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Transcriptional profile of monocytes in the colon in response to C. rodentium infection Overall design: Eight samples have been analyzed. All are from Cd11b+Ly6C+ inflammatory monocytes sorted from colonic tissue 9 days after C. rodentium infection from Atg16L1HM(4) and WT(4) mice.

Publication Title

Autophagy proteins suppress protective type I interferon signalling in response to the murine gut microbiota.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE75994
Expression data comparing Hep3B Caveolin-1 (Cav1) knockdown cells with Hep3B non-target control cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To identify genes regulated by Cav1

Publication Title

Mechanisms through Which Hypoxia-Induced Caveolin-1 Drives Tumorigenesis and Metastasis in Hepatocellular Carcinoma.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE115635
Systematic Identification of EpithelialStromal Crosstalk Signaling Networks in Ovarian Cancer
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Ovarian cancer is the most lethal malignancy in the United States. While studies on ovarian cancer pathogenesis were mainly focused on the epithelial component of the tumor, understanding in the role of cancer associated fibroblasts (CAFs) in ovarian cancer progression is limited. In the present study, we describe the use of microdissected transcriptome profiles for the identification of cancerstroma crosstalk networks with prognostic value, which presents a unique opportunity for developing new treatment strategies for ovarian cancer.

Publication Title

Systematic Identification of Druggable Epithelial-Stromal Crosstalk Signaling Networks in Ovarian Cancer.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE46209
Non-telomeric role for Rap1 in regulating metabolism and protecting against obesity
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The mammalian telomere-binding protein Rap1 was found to have additional non-telomeric functions, acting as a transcriptional cofactor and a regulator of the NF-kB pathway. Here, we assess the effect of disrupting mouse Rap1 in vivo, and report on its unanticipated role in metabolic regulation and body weight homeostasis. Rap1 inhibition causes dysregulation in hepatic as well as adipose function. In addition, using a separation-of-function allele, we show that the metabolic function of Rap1 is independent of its recruitment to TTAGGG binding elements found at telomeres, and at other interstitial loci.

Publication Title

Nontelomeric role for Rap1 in regulating metabolism and protecting against obesity.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE34042
Global methylation analysis identifies PITX2 as an upstream regulator of the androgen receptor and IGF-I receptor genes in prostate cancer
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The insulin-like growth factor-I (IGF-IR) and androgen (AR) receptors are important players in prostate cancer biology. Functional interactions between the IGF-I and androgen signaling pathways seem to have crucial roles in the progression of prostate cancer from early (benign) to advanced (metastatic) stages. DNA methylation is a major epigenetic alteration affecting gene expression. Hypermethylation of tumor suppressor promoters is a frequent event in human cancer, leading to inactivation and repression of specific genes. The aim of the present study was to identify the entire set of methylated genes (methylome) in a cellular model that replicates prostate cancer progression.

Publication Title

Global methylation analysis identifies PITX2 as an upstream regulator of the androgen receptor and IGF-I receptor genes in prostate cancer.

Sample Metadata Fields

Cell line, Treatment, Time

View Samples
accession-icon GSE32309
Sustained axon regeneration induced by a synergy of PTEN and SOCS3 deletion
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

A formidable challenge in neural repair in the adult central nervous system (CNS) is the long distances that regenerating axons often need to travel in order to reconnect with their targets. Thus, a sustained capacity for axon regeneration is critical for achieving functional restoration. Although deletion of either Phosphatase and tensin homolog (PTEN), a negative regulator of mammalian target of rapamycin (mTOR), or suppressor of cytokine signaling 3 (SOCS3), a negative regulator of Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, in adult retinal ganglion cells (RGCs) individually promoted significant optic nerve regeneration, such regrowth tapered off around two weeks after the crush injury. Remarkably, we now find that simultaneous deletion of both PTEN and SOCS3 enable robust and sustained axon regeneration. We further show that PTEN and SOCS3 regulate two independent pathways that act synergistically to promote enhanced axon regeneration. Gene expression analyses suggest that double deletion not only result in the induction of many growth-related genes, but also allow RGCs to maintain the expression of a repertoire of genes at the physiological level after injury. Our results reveal concurrent activation of mTOR and STAT3 pathways as a key for sustaining long-distance axon regeneration in adult CNS, a crucial step toward functional recovery.

Publication Title

Sustained axon regeneration induced by co-deletion of PTEN and SOCS3.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE54175
Identification of chemoresistant genes in hepatocellular carcinoma (HCC)
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The aim of this study was to identify chemoresistance-associated genes in hepatocellular carcinoma (HCC).

Publication Title

Identification of transmembrane protein 98 as a novel chemoresistance-conferring gene in hepatocellular carcinoma.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Cell line

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accession-icon GSE14712
Xenobiotic-responsive Nuclear Receptors in Transcriptional Effects Upon Perfluoroalkyl Acid Exposure in Diverse Species
  • organism-icon Rattus norvegicus
  • sample-icon 129 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a)

Description

Humans and ecological species have been found to have detectable body burdens of a number of perfluorinated alkyl acids (PFAA) including perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS). In mouse and rat liver these compounds elicit transcriptional and phenotypic effects similar to peroxisome proliferator chemicals (PPC) that work through the nuclear receptor peroxisome proliferator activated receptor alpha (PPARalpha). Recent studies indicate that along with PPARalpha other nuclear receptors are required for transcriptional changes in the mouse liver after PFOA exposure including the constitutive activated receptor (CAR) and pregnane X receptor (PXR) that regulate xenobiotic metabolizing enzymes (XME). To determine the potential role of CAR/PXR in mediating effects of PFAAs in rat liver, we performed a meta-analysis of transcript profiles from published studies in which rats were exposed to PFOA or PFOS. We compared the profiles to those produced by exposure to prototypical activators of CAR (Phenobarbital (PB)), PXR (pregnenolone 16 alpha-carbonitrile (PCN)), or PPARalpha (WY-14,643 (WY)). As expected, PFOA and PFOS elicited transcript profile signatures that included many known PPARalpha target genes. Numerous XME genes were also altered by PFOA and PFOS but not WY. These genes exhibited expression changes shared with PB or PCN. Reexamination of the transcript profiles from the livers of chicken or fish exposed to PFAAs indicated that PPARalpha, CAR, and PXR orthologs were not activated. Our results indicate that PFAAs under these experimental conditions activate PPARalpha, CAR, and PXR in rats but not chicken and fish. Lastly, we discuss evidence that human populations with greater CAR expression have lower body burdens of PFAAs.

Publication Title

Evidence for the involvement of xenobiotic-responsive nuclear receptors in transcriptional effects upon perfluoroalkyl acid exposure in diverse species.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE40595
A cancer associated fibroblasts (CAFs) specific gene signature in high grade serous ovarian cancer
  • organism-icon Homo sapiens
  • sample-icon 72 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Ovarian cancer is the most lethal malignancy in the United States. In the year 2012, there will be an estimated 22,280 new cases and 15,500 deaths from ovarian cancer in the country (Siegel et al., 2012). While studies on ovarian cancer pathogenesis were mainly focused on the epithelial component of the tumor, understanding in the role of cancer associated fibroblasts (CAFs) in ovarian cancer progression is limited. We hypothesized that comparing the gene expression profiles of different components from laser capture microdissected ovarian tissue will allow us to identify an ovarian CAFs specific gene signature which accounts for the supportive role of CAFs in ovarian cancer progression. In this study, gene expression profiling was completed for 31 cancer stroma samples and 32 samples of epithelial component from high grade serous ovarian cancer patients. 8 microdissected normal ovarian stroma and 6 normal human ovarian surface epithelium (HOSE) samples were also included in the study. By comparing the expression data from cancer stroma against that from normal stroma, cancer cells and HOSE, we identified a set of differential expressed genes in ovarian CAFs which showed correlation with cancer patient survival. Further study on these genes can reveal their roles in ovarian cancer progression and pathogenesis. Ultimately, ovarian CAFs specified genes identified in this study may aid in the classification and enhancement of patient outcome.

Publication Title

TGF-β modulates ovarian cancer invasion by upregulating CAF-derived versican in the tumor microenvironment.

Sample Metadata Fields

Specimen part

View Samples

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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