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accession-icon GSE64686
Expression data from the inducible expression of EWS-FLI1 (EF) in embryoid bodies
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Oncogenic transformation in Ewing sarcoma tumors is driven by the fusion oncogene EWS-FLI1. The inducible expression of EWS-FLI1 (EF) in embryoid bodies, or collections of differentiating stem cells, generates cells with properties of Ewing sarcoma tumors, including characteristics of transformation. These cell lines exhibit anchorage-independent growth, a lack of contact inhibition and a strong Ewing sarcoma gene expression signature. These cells also demonstrate a requirement for the persistent expression of EWS-FLI1 for cell survival and growth.

Publication Title

Modeling the initiation of Ewing sarcoma tumorigenesis in differentiating human embryonic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon SRP067963
Transcriptome profiling of post-mature green seeds from Arabidopsis ddcc mutant and wild-type
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The role of on-CG methylation in seed development and dormancy remains unknown. There are four genes in charge of non-CG methylation in Arabidopsis: drm1, drm2, cmt2 and cmt3. The majority of non-CG methylation in vegetative tissues, leaf, is gone in homozygous ddcc mutant line (Hume et al., 2014). To uncover the possible role of non-CG DNA methylation in seed development and dormancy, we characterized the transcriptome of ddcc mutant in Arabidopsis post-mature green seeds using Illumina sequencing. Meanwhile, post-mature green seeds from wild type were used as control. Overall design: Illumina sequencing of transcripts from post-mature green seeds of ddcc mutant and wild type. Two biological replicates were collected.

Publication Title

Similarity between soybean and <i>Arabidopsis</i> seed methylomes and loss of non-CG methylation does not affect seed development.

Sample Metadata Fields

Specimen part, Subject

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accession-icon E-MEXP-822
Transcription profiling by array of diploid and tetraploid S. cerevisiae cultures
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Diploid and tetraploid budding yeast cell cultures were grown in YPD, at 30C, to O.D. approx. 0.5.

Publication Title

Genome-wide genetic analysis of polyploidy in yeast.

Sample Metadata Fields

Sex

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accession-icon GSE57864
Gene expression in diploid and evolved tetraploid RPE-1 and BJ-1 cells
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Both diploid RPE-1 and BJ-1 cells were made tetraploid by transient treatment with the cytokinesis inhibitor DCD. Proliferating tetraploids from both BJ-1 and RPE-1 were selected and isolated. The gene expression profiles of the proliferating tetraploid cells were then compared to the diploids from which they originated.

Publication Title

Cytokinesis failure triggers hippo tumor suppressor pathway activation.

Sample Metadata Fields

Specimen part

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accession-icon GSE57769
Gene expression profile of diploid and tetraploid mouse primary hepatocyte
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Genetically unstable tetraploid cells can promote tumorigenesis. Recent estimates suggest that ~37% of human tumors have undergone a genome-doubling event during their development. This potentially oncogenic effect of tetraploidy is countered by a p53-dependent barrier to proliferation. However, the cellular defects and corresponding signaling pathways that trigger growth suppression in tetraploid cells are not known. Here we combine genome-scale RNAi screening and in vitro evolution approaches to demonstrate that cytokinesis failure activates the Hippo tumor suppressor pathway in cultured cells as well as in naturally occurring tetraploid cells in vivo. Induction of the Hippo pathway is triggered in part by extra centrosomes, which alter small G-protein signaling and activate LATS2 kinase; LATS2 in turn stabilizes p53 and inhibits the transcriptional regulators YAP and TAZ. These findings define an important tumor suppression mechanism. Furthermore, our experiments uncover adaptations that allow nascent tumor cells to bypass this inhibitory regulation.

Publication Title

Cytokinesis failure triggers hippo tumor suppressor pathway activation.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP067454
Myc-dependent gene activation and repression in oncogene-addicted liver tumors (RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 43 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Tumors driven by activation of the transcription factor Myc generally show oncogene addiction. However, the gene-expression programs that depend upon sustained Myc activity in those tumors remain unknown. We have addressed this issue in a model of liver carcinoma driven by a reversible tet-Myc transgene, combining gene expression profiling with the mapping of Myc and RNA Polymerase II on chromatin. Switching off the oncogene in advanced carcinomas revealed that Myc is required for the continuous activation and repression of distinct sets of genes, constituting no more than half of those deregulated during tumor progression, and an even smaller subset of all Myc-bound genes. We further showed that a Myc mutant unable to associate with the co-repressor protein Miz1 is defective in the initiation of liver tumorigenesis. Altogether, our data provide the first detailed analysis of a Myc-dependent transcriptional program in a fully developed carcinoma, revealing that the critical effectors of Myc in tumor maintenance must be included within defined subsets (ca. 1,300 each) of activated and repressed genes. Overall design: RNAseq samples of control liver (n=11), tet-Myc tumors (n=16), tet-Myc tumors with short-term Myc inactivation (n=8), tet-MycVD tumors (n=11)

Publication Title

Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE22392
Expression data from hESCs, hiPSCs and human fibroblasts.
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Detailed analysis comparing hiPSC lines that were newly generated and compared them to already established hiPSC lines

Publication Title

Molecular analyses of human induced pluripotent stem cells and embryonic stem cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE76765
Tumor Cell Survival Dependence on the DExH-Box Helicase DHX9
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

The ATP-dependent DExH/D-box helicase DHX9 is a key participant in a number of gene regulatory steps, including transcriptional, translational, microRNA-mediated control, DNA replication, and maintenance of genomic stability. DHX9 has also been implicated in maintenance of the tumorigenic process and in drug response. Here, we report that inhibition of DHX9 expression is lethal to multiple human and mouse cancer cell lines. In contrast, using a novel conditional shDHX9 mouse model, we demonstrate that sustained and prolonged suppression of DHX9 is well tolerated at the organismal level. Our results demonstrate a robust tolerance for DHX9 knockdown in non-transformed cells and supports the targeting of DHX9 as an effective and specific chemotherapeutic approach.

Publication Title

Tumor cell survival dependence on the DHX9 DExH-box helicase.

Sample Metadata Fields

Specimen part

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accession-icon SRP164926
Trisomy of a 'Down syndrome critical region' globally amplifies transcription via HMGN1 overexpression [SLAM-Seq]
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Down syndrome (DS, trisomy 21) is associated with developmental abnormalities and increased leukemia risk. To reconcile chromatin alterations with transcriptome changes in cells with trisomy 21, we performed paired exogenous spike-in normalized RNA and chromatin immunoprecipitation sequencing in DS models. Absolute per cell normalization unmasked global amplification of gene expression associated with trisomy 21. Overexpression of the nucleosome binding protein HMGN1 (encoded on chr21q22) recapitulated the transcriptional changes seen with triplication of a “Down syndrome critical region” on distal chromosome 21. Absolute exogenous normalized ChIP-seq (ChIP-Rx) also revealed a global increase in histone 3 lysine 27 acetylation caused by HMGN1. Genes most amplified downstream of HMGN1 were enriched for tumor- and developmental stage-specific programs of B-cell acute lymphoblastic leukemia dependent on the cellular context. These data offer a mechanistic explanation for DS transcriptional patterns, and suggest that further study of HMGN1 and RNA amplification in diverse DS phenotypes is warranted. Overall design: SLAM-seq in NALM6 human pre-B cells with engineered HMGN1 overexpression

Publication Title

Trisomy of a Down Syndrome Critical Region Globally Amplifies Transcription via HMGN1 Overexpression.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon SRP131037
Using Next-Generation Sequencing Transcriptomics to Determine Markers of Post-traumatic Symptoms - preliminary findings from a post-deployment cohort
  • organism-icon Homo sapiens
  • sample-icon 78 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Post-traumatic stress disorder is a concerning psycho behavioral disorder thought to emerge from the complex interaction between genetic and environmental factors. For soldiers exposed to combat, the risk of developing this disorder is two-fold and diagnosis is often late, when much sequela has set in. To be able to identify and diagnose in advance those at “risk” of developing PTSD, would greatly taper the gap between late sequelae and treatment. Therefore, this study sought to test the hypothesis that the transcriptome can be used to track the development of PTSD in this unique and susceptible cohort of individuals. Gene expression levels in peripheral blood samples from 85 Canadian infantry soldiers (n = 58 subjects negative for PTSD symptoms and n = 27 subjects with PTSD symptoms) were determined by RNA sequencing technology following their return from deployment to Afghanistan. Count-based gene expression quantification, normalization and differential analysis (with thorough correction for confounders) revealed significant differences in two genes, LRP8 and GOLM1 . These preliminary results provide a proof-of-principle for the diagnostic utility of blood-based gene expression profiles for tracking symptoms of post-traumatic stress disorder in soldiers returning from tour. It is also the first to report transcriptome-wide expression profiles alongside a post-traumatic symptom checklist. Overall design: Peripheral blood samples from 85 Canadian infantry soldiers (n = 58 subjects negative for PTSD symptoms and n = 27 subjects with PTSD symptoms)

Publication Title

Using Next-Generation Sequencing Transcriptomics To Determine Markers of Post-traumatic Symptoms: Preliminary Findings from a Post-deployment Cohort of Soldiers.

Sample Metadata Fields

Sex, Subject

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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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