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accession-icon SRP144750
Stromal Fibroblasts Drive Single Cell Heterogeneity in Pancreatic Cancer
  • organism-icon Homo sapiens
  • sample-icon 188 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To understand the interplay between cancer and stroma, we performed single cell RNA-sequencing of PDAC cells admixed with stromal fibroblasts and defined different single cell populations with varying levels of proliferative and metastatic transcriptional states. PDAC cell behavior in vitro and in vivo on these phenotypic axes could be tuned with the proportion of stromal fibroblasts. These cell types were identified in human pancreatic tumors, and specific subpopulations were associated with worsened outcomes. Overall design: 92 single PDAC cells and 92 single CAF cells were micromanipulated and prepared for sequencing (23 of each cell type from four culture ratios). The 24th sample from each cell type-culture condition combination is a population control obtained by micromanipulating 100 cells of the given type from the given culture condition and preparing it as if it were a single cell, giving a total of 96 PDAC samples and 96 CAF samples. During the course of library construction, 3 samples were lost, all PDAC cells from the 30:70 condition (two single cells and the population control), leaving 93 total PDAC samples and 96 total CAF samples.

Publication Title

Stromal Microenvironment Shapes the Intratumoral Architecture of Pancreatic Cancer.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE2531
JEG3 vs BeWo
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

In this experiment we compared total RNA from two commonly used choriocarcinoma cell lines, JEG3 and BeWo, to identify differentially expressed transcripts.

Publication Title

Microarray analysis of BeWo and JEG3 trophoblast cell lines: identification of differentially expressed transcripts.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP059066
Combinatorial Regulation Mediated by Biochemically Distinct Forms of SWI/SNF [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

The precise makeup of chromatin remodeling complexes is important for determining cell type and cell function. The SWI/SNF chromatin remodeling complex is made up of multiple subunits that can be filled by mutually exclusive proteins. Inclusion or exclusion of these proteins has profound functional consequences, yet we currently understand little about the direct functional relationship between these biochemically distinct forms of remodeling complexes. Here we combine chromatin immunoprecipitation, transcriptome analysis, and transcription factor binding information from the ENCODE project to determine the functional relationship between three biochemically distinct forms of SWI/SNF. We find widespread overlap in transcriptional regulation and the genomic binding of the three ARID (AT-Rich Interacting Domain) subunits of SWI/SNF. Despite the numerous similarities in their transcriptional regulation and the co-factors bound with each ARID we identify several novel interaction modalities. Previous work has found examples of competition or subunit switching at individual loci, and we find this functional relationship is widespread, and in these cases gene expression changes following loss of one ARID depend on the function of another ARID. We also identify a previously unknown cooperative interaction between ARID1B and ARID2 in the repression of a large number of genes. Together these data help untangle the complicated combinatorial relationships between a highly heterogenous chromatin remodeling family. Overall design: We performed depletion of ARID subunits (ARID1A , n=5; ARID1B, n=3, ARID2, n=5) of SWI/SNF using siRNA or a Non-Targeting control (N=6) and performed expression analysis using polyA+ selected RNA and a strand-specific dUTP incorporation library protocol.

Publication Title

Genome-Wide Transcriptional Regulation Mediated by Biochemically Distinct SWI/SNF Complexes.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP164908
Tumor-infiltrating immune cells of young and aged mice
  • organism-icon Mus musculus
  • sample-icon 74 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Macrophages, dendritic cells, conventional CD4+ T cells, CD8+ T cells, and regulatory T cells isolated from mouse colon cancer model MC38 tumors implanted subcutaneously to young (3 month) and aged (12 month) mice were sequenced using ImmGen's standard ultra-low input RNA-seq pipeline, in order to study age-dependent differences in intraltumoral immune cell functions and their impact on tumor control Overall design: Samples collected at the Center for Systems Biology at Mass General Hospital, shipped frozen to a central location, and sequenced using ImmGen's standard RNA-seq pipeline

Publication Title

Age-related tumor growth in mice is related to integrin α 4 in CD8+ T cells.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon SRP059364
Histone H3.3 maintains genome integrity during mammalian development
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Histone H3.3 is a highly conserved histone H3 replacement variant in metazoans, and has been implicated in many important biological processes including cell differentiation and reprogramming. Germline and somatic mutations in H3.3 genomic incorporation pathway components, or in H3.3 encoding genes, have been associated with human congenital diseases and cancers, respectively. However, the role of H3.3 in mammalian development remains unclear. To address this question, we generated H3.3 null mouse models through classical genetic approaches. We found H3.3 plays an essential role in mouse development. Complete depletion of H3.3 leads to developmental retardation and early embryonic lethality. At the cellular level, H3.3 loss triggers cell cycle suppression and cell death. Surprisingly, H3.3 depletion does not dramatically disrupt gene regulation in the developing embryo. Instead, H3.3 depletion causes dysfunction of heterochromatin structures at telomeres, centromeres and pericentromeric regions of chromosomes leading to mitotic defects. The resulting karyotypical abnormalities and DNA damage lead to p53 pathway activation. In summary, our results reveal that an important function of H3.3 is to support chromosomal heterochromatic structures, thus maintaining genome integrity during mammalian development. Overall design: RNA-seq in embryos at E10.5 comparing 3 samples with the following genotype Trp53-/-; H3f3afl/-; H3f3bfl/-; Sox2-CreTg/0 to three samples with the following genotype Trp53-/-; H3f3afl/+; H3f3bfl/+; Sox2-CreTg/0

Publication Title

Histone H3.3 maintains genome integrity during mammalian development.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP105353
Long Noncoding RNA Moderates microRNA Activity to Maintain Self-Renewal in Embryonic Stem Cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Of the thousands of long non-coding RNAs expressed in embryonic stem (ES) cells, few have known roles and fewer have been functionally implicated in the regulation of self-renewal and pluripotency or reprogramming somatic cells to the pluripotent state. In ES cells, Cyrano is a stably expressed long intergenic non-coding RNA with no previously assigned role. We demonstrate that Cyrano contributes to ES cell maintenance, as its depletion results in loss of hallmarks of self-renewal. Delineation of Cyrano''s network through transcriptomics revealed widespread effects on signaling pathways and gene expression networks that contribute to ES cell maintenance. Cyrano shares unique sequence complementarity with the differentiation-associated microRNA, mir-7, and mir-7 overexpression reduces expression of a key self-renewal factor to a similar extent as Cyrano knockdown. This suggests that Cyrano functions to restrain the action of mir-7. Altogether, we provide a view into the multifaceted function of Cyrano in ES cell maintenance. Overall design: RNA-seq on mouse R1 embryonic stem (ES) cells with two biological replicates transfected with an shRNA knockdown of Cyrano and two biological replicates transfected with a non-targeting control vector.

Publication Title

Long Noncoding RNA Moderates MicroRNA Activity to Maintain Self-Renewal in Embryonic Stem Cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE24369
Gene expression profiling of low-grade fibromyxoid sarcoma (LGFMS)
  • organism-icon Homo sapiens
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Analysis of gene expression in 17 low-grade fibromyxoid sarcoma (LGFMS) samples compared to that of histologically similar tumors. LGFMS is characterized by the specific translocations t(7;16)(q33;p11) or t(11;16)(p11;p11) and corresponding fusion genes FUS-CREB3L2 or FUS-CREB3L1.

Publication Title

FUS-CREB3L2/L1-positive sarcomas show a specific gene expression profile with upregulation of CD24 and FOXL1.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE41509
Yap role in intestine
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Restriction of intestinal stem cell expansion and the regenerative response by YAP.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE41507
RSpondin1 treatment of control and Yap cKO mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

RSpondin1 adenovirus was administered to mice and intestine was isolated for expression analysis 1 week later.

Publication Title

Restriction of intestinal stem cell expansion and the regenerative response by YAP.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE61093
Loss of the tumor suppressor gene AIP mediates the browning of human brown fat tumors
  • organism-icon Homo sapiens
  • sample-icon 85 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Human brown fat tumors (hibernomas) display concomitant loss of the tumor suppressor genes MEN1 and AIP. In the present study, we hypothesized that the brown fat phenotype is attributed to these mutations. Accordingly, we demonstrate that silencing of AIP in human brown preadipocytic and white fat cell lines results in the induction of the brown fat marker UCP1. In human adipocytic tumors, loss of MEN1 was found both in white (one out of 51 lipomas) and brown fat tumors. In contrast, concurrent loss of AIP was always accompanied by a brown fat morphology. We conclude that this white-to-brown phenotype switch in brown fat tumors is mediated by the loss of AIP.

Publication Title

Loss of the tumour suppressor gene AIP mediates the browning of human brown fat tumours.

Sample Metadata Fields

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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