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accession-icon GSE28015
Identification of Tumor Suppressors and Oncogenes from Genomic and Epigenetic Features in Ovarian Cancer
  • organism-icon Homo sapiens
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Identification of tumor suppressors and oncogenes from genomic and epigenetic features in ovarian cancer.

Sample Metadata Fields

Sex, Disease, Disease stage, Treatment

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accession-icon GSE41678
System-Wide Analysis Reveals a Complex Network of Tumor-Fibroblast Interactions Involved in Tumorigenicity
  • organism-icon Homo sapiens
  • sample-icon 79 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Weve undertaken a genome-wide approach to identify and test genes in fibroblasts that are both induced upon interaction with basal breast cancer cells in culture and upregulated in stromal cells from primary human breast cancers. Several of the upregulated genes encode secreted growth factors or cytokines. Using RNAi and a co-injection tumorigenicity assay, we determined that the majority of secreted factors selected for functional validation played significant, yet functionally diverse, roles in promoting tumorigenicity. Rather than a single major mediator, these results indicate multiple points of intervention to prevent fibroblasts from supporting basal breast cancer. Additionally, we show that breast cancer subtypes differ markedly in the expression of these and other stromally secreted proteins using data from microdissected stromal samples.

Publication Title

System-wide analysis reveals a complex network of tumor-fibroblast interactions involved in tumorigenicity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE27943
Gene Expression Array of Human Ovarian Cancer.
  • organism-icon Homo sapiens
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The identification of genetic and epigenetic alterations from primary tumor cells has become a common method to identify genes critical to the development and progression of cancer. We provide a bioinformatic analysis of copy number variation and DNA methylation covering the genetic landscape of ovarian cancer tumor cells. We individually examined the copy number variation and DNA methylation for 44 primary ovarian cancer samples and 7 ovarian normal samples using our MOMA-ROMA technology and Affymetrix expression data as well as 379 tumor samples analyzed by The Cancer Genome Atlas. We have identified 346 genes with significant deletions or amplifications among the tumor samples. Utilizing associated gene expression data we predict 156 genes with significantly altered copy number and correlated changes in expression. We identify changes in DNA methylation and expression for all amplified and deleted genes. We predicted 615 potential oncogenes and tumor suppressors candidates by integrating these multiple genomic and epigenetic data types.

Publication Title

Identification of tumor suppressors and oncogenes from genomic and epigenetic features in ovarian cancer.

Sample Metadata Fields

Sex, Disease, Disease stage

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accession-icon GSE37055
Cell-type specific postnatal developmental expression data from mouse cerebellar Purkinje and Stellate/Basket cells
  • organism-icon Mus musculus
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The assembly of neural circuits involves multiple sequential steps such as the specification of cell types, their migration to proper brain locations, morphological and physiological differentiation, and the formation and maturation of synaptic connections. This intricate and often prolonged process is guided by elaborate genetic mechanisms that regulate each developmental event. Evidence from numerous systems suggests that each cell type, once specified, is endowed with a genetic program that directs its subsequent development. This cell intrinsic program unfolds in respond to, and is regulated by, extrinsic signals, including cell-cell and synaptic interactions. To a large extent, the execution of this genetic program is achieved by the expression of specific sets of genes that support distinct developmental processes. Therefore, a comprehensive analysis of the developmental progression of gene expression in synaptic partners of neurons may provide a basis for exploring the genetic mechanisms regulating circuit assembly.

Publication Title

Developmental Coordination of Gene Expression between Synaptic Partners During GABAergic Circuit Assembly in Cerebellar Cortex.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE32012
Dosage-dependent phenotypes in models of 16p11.2 lesions found in autism
  • organism-icon Mus musculus
  • sample-icon 37 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Recurrent Copy Number Variations (CNVs) of human 16p11.2 have been associated with a variety of developmental/neurocognitive syndromes. In particular, deletion of 16p11.2 is found in patients with autism, developmental delay, and obesity. Patients with deletions or duplications have a wide range of clinical features, and siblings carrying the same deletion often have diverse symptoms. To study the consequence of 16p11.2 CNVs in a systematic manner, we used chromosome engineering to generate mice harboring deletion of the chromosomal region corresponding to 16p11.2, as well as mice harboring the reciprocal duplication. These 16p11.2 CNV models have dosage-dependent changes in gene expression, viability, brain architecture, and behavior. For each phenotype, the consequence of the deletion is more severe than that of the duplication. Of particular note is that half of the 16p11.2 deletion mice die postnatally; those that survive to adulthood are healthy and fertile, but have alterations in the hypothalamus and exhibit a behavior trap phenotypea specific behavior characteristic of rodents with lateral hypothalamic and nigrostriatal lesions. Our findings indicate that 16p11.2 CNVs cause both brain and behavioral anomalies, providing new insight into human neurodevelopmental disorders.

Publication Title

Dosage-dependent phenotypes in models of 16p11.2 lesions found in autism.

Sample Metadata Fields

Sex

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accession-icon GSE52952
miRNAs trigger widespread epigenetically-activated siRNAs from transposons in Arabidopsis
  • organism-icon Arabidopsis thaliana
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

miRNAs trigger widespread epigenetically activated siRNAs from transposons in Arabidopsis.

Sample Metadata Fields

Specimen part

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accession-icon GSE27222
Gene expression data for the budding yeast mutants pol30-8, dot1 and pol30-8 dot1
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

The mutation in the budding yeast gene PCNA, pol30-8, as well as deletion of DOT1 (dot1), encoding the only histone H3 K79 methyltransferase in budding yeast, have been implicated in telomeric silencing. To further analyze these mutants, we used microarrays to study whether either pol30-8, dot1 or the double mutant leads to changes in gene expression levels when compared to isogenic wild-type strains.

Publication Title

A common telomeric gene silencing assay is affected by nucleotide metabolism.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE36141
Gene expression data at 24hrs post-siRNA transfection for HCT116 cultures transfected with either DDX5si2008, DDX5si2053, or EBNA1si1666 siRNA's or mock transfected.
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

HCT116 cells were transfected with two different siRNA's targeting either DDX5, an siRNA targeting EBNA1, or no siRNA (mock). The siRNA targeting EBNA1 is used as a negative control since HCT116 cells do not have the EBNA1 gene. RNA was obtained from cultures at 24hrs post-siRNA transfection using the Qiagen RNeasy Minikit (cat. # 74104) with on-column DNase digestion performed as per the manufacturer's protocol. The RNA samples were isolated at 24hrs post-siRNA transfection since this timepoint precedes an impaired G1-to-S phase cell cycle progression phenotype that is evident at 48hrs post-siRNA transfection and so may reveal gene expression changes occuring before this effect on cell cycle. RNA samples were submitted to the Cold Spring Harbor Laboratory Microarray Faciity where cDNA was prepared, labeled, and hybridized to Affymetrix GeneChip Human Gene 1.0 ST microarrays. Data from the arrays were processed using the RMA method with an up-to-data probe set definition (Biostatistics 4:249-264 and Nucleic Acids Research 33(20):e175. Gene set analysis was performed using generally applicable gene set enrichment (BMC Bioinformatics 10:161). The most differentially regulated gene ontology groups were selected with FDR q-value < 0.1.

Publication Title

DDX5 regulates DNA replication and is required for cell proliferation in a subset of breast cancer cells.

Sample Metadata Fields

Cell line

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accession-icon GSE30987
Identification of PHLPP1 as a tumor suppressor reveals the role of feedback compensation in PTEN-mutant prostate cancer progression
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Hyper-activation of the PI 3-Kinase/ AKT pathway is a driving force of many cancers. Here we identify the AKT-inactivating phosphatase PHLPP1 as a prostate tumor suppressor. We show that Phlpp1-loss causes neoplasia and, upon partial Pten-loss, carcinoma in mouse prostate. This genetic setting initially triggers a growth suppressive response via p53 and the Phlpp2 ortholog, and reveals spontaneous Trp53 inactivation as a condition for full-blown disease. Surprisingly, the co-deletion of PTEN and PHLPP1 in patient samples is highly restricted to metastatic disease and tightly correlated to deletion of TP53 and PHLPP2. These data establish a conceptual framework for progression of PTEN-mutant prostate cancer to life-threatening disease.

Publication Title

No associated publication

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE52067
miRNAs trigger widespread epigenetically-activated siRNAs from transposons inArabidopsis [Affymetrix]
  • organism-icon Arabidopsis thaliana
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Utilizing Affymetrix ATH1 microarrays to analyze transposon expression in DNA methylation mutants, and RNAi mutants, compared to wildtype.

Publication Title

miRNAs trigger widespread epigenetically activated siRNAs from transposons in Arabidopsis.

Sample Metadata Fields

Specimen part

View Samples
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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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