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accession-icon GSE111580
Expression data in non-tumor liver tissues from Peruvian patients with hepatocellular carcinoma.
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Most hepatocellular carcinomas in younger patients from Peru arise from non-cirrhotic livers. Histological examination of the non-tumor liver tissues highlights the presence of clear cell foci in a significant fraction of Peruvian patients with hepatocellular carcinoma.

Publication Title

Liver clear cell foci and viral infection are associated with non-cirrhotic, non-fibrolamellar hepatocellular carcinoma in young patients from South America.

Sample Metadata Fields

Specimen part, Disease stage, Subject

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accession-icon GSE41892
Tetraspanin TSPAN12 regulates tumor growth and metastasis and inhibits -catenin degradation
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Ablation of tetraspanin protein TSPAN12 from human MDA-MB-231 cells significantly decreased primary tumor xenograft growth, while increasing tumor apoptosis. Furthermore, TSPAN12 removal markedly enhanced tumor-endothelial interactions and increased metastasis to mouse lungs. TSPAN12 removal from human MDA-MB-231 cells also caused diminished association between FZD4 (a key canonical Wnt pathway receptor) and its co-receptor LRP5. The result likely explains substantially enhanced proteosomal degradation of -catenin, a key effecter of canonical Wnt signalling. Consistent with disrupted canonical Wnt signaling, TSPAN12 ablation altered expression of LRP5, Naked 1 and 2, DVL2, DVL3, Axin 1 and GSK3 proteins. TSPAN12 ablation also altered expression of several genes regulated by -catenin (e.g. CCNA1, CCNE2, WISP1, ID4, SFN, ME1) that may help to explain altered tumor growth and metastasis. In conclusion, these results provide the first evidence for TSPAN12 playing a role in supporting primary tumor growth and suppressing metastasis. TSPAN12 appears to function by stabilizing FZD4-LRP5 association, in support of canonical Wnt-pathway signaling, leading to enhanced -catenin expression and function.

Publication Title

Tetraspanin TSPAN12 regulates tumor growth and metastasis and inhibits β-catenin degradation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37448
Immunological Genome Project data Phase 2
  • organism-icon Mus musculus
  • sample-icon 181 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Gene-expression microarray datasets generated as part of the Immunological Genome Project (ImmGen) for samples that use a different set of amplification reagents (Ambion WT Expression Kit, not the Affymetrix GeneChip WT cDNA Synthesis and Amplification Kits).

Publication Title

The tumor microenvironment shapes lineage, transcriptional, and functional diversity of infiltrating myeloid cells.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE14380
Gastrointestinal differentiation marker Cytokeratin 20 is regulated by homeobox gene CDX1
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This study is to identify downstream targets of homeobox gene CDX1. The study assayed the expression of 2 pairs of stably transfected colorectal cancer cell lines: The CDX1 nonexpressing CRC cell line HCT116 was stably transfected with either CDX1 cDNA in the pRC/CMV expression vector (HCT116-CDX1) or with vector control (HCT116-Vec). The CDX1-expressing CRC cell line LS174T was similarly transfected with either a pSilencer vector containing a short sequence of CDX1 siRNA (LS174T-siRNA) , or a pSilencer vector containing a scrambled siRNA sequence as a control (LS174T-Vec).

Publication Title

Gastrointestinal differentiation marker Cytokeratin 20 is regulated by homeobox gene CDX1.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE85
wild type and aire -/- murine meduallary thymic epithelial cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Mice used were B6/129 F2's, 3-5 weeks of age, either wild type or with both copies of the autoimmune regulator gene (aire, GenBank #AF079536) disrupted. Thymi from five of these mice of both sexes were removed and pooled. After collagenase/dispase digestion, density gradient fractionation, and fluorescent antibody staining, cells with the phenotype CD45-, G8.8+, CDR1int and B7.1hi were FACS-sorted and total RNA was made from them. RNA was twice-amplified using a T7 polymerase-based method.

Publication Title

Projection of an immunological self shadow within the thymus by the aire protein.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP042009
RNA-seq of mouse ES cells depleted of MOF, MSL1, MSL2 or KANSL3
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We have studied the regulatory potential of MYST1-(MOF)-containing MSL and NSL complexes in mouse embryonic stem cells (ESCs) and neuronal progenitors. We find that both complexes influence transcription by binding to promoters as well as TSS-distal enhancer regions. In contrast to flies, the MSL complex is not enriched on the X chromosome yet it is crucial for mammalian X chromosome regulation as it specifically regulates Tsix ncRNA, the major repressor of Xist lncRNA. MSL depletion leads to severely decreased Tsix expression, reduced REX1 recruitment, and consequently accumulation of Xist RNA in ESCs. The NSL complex provides additional, Tsix-independent repression of Xist by maintaining pluripotency. MSL and NSL complexes therefore act synergistically by using distinct pathways to ensure a fail-safe mechanism for the repression of X inactivation in ESCs. Overall design: We have performed ChIP-seq of KANSL3, MCRS1, MOF, MSL1 and MSL2 in mouse ESCs, and KANSL3, MOF and MSL2 in NPCs, in duplicate and normalised against their inputs. We have also performed RNA-seq following knockdown of Kansl3, Mof, Msl1 and Msl2 mouse embryonic stem cells in triplicate. NB: Kansl3 and Mof knockdown-RNAseq are analyzed against their own scrambled controls, and Msl1 and Msl2 against another scrambled control triplicate. siMCRS1 & siMOF were compared to scrambled1 (scr1) siMsl1 and siMsl2 were compared to scr2 siNsl3 was compared to scr3

Publication Title

MOF-associated complexes ensure stem cell identity and Xist repression.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE22083
Expression data from human skin exposed to solar-simulated radiation with or without sunscreen
  • organism-icon Homo sapiens
  • sample-icon 98 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Despite widespread use of sunscreens that minimize erythema by blocking ultraviolet B (UVB) radiation, incidence rates of melanoma continue to rise. In considering this disparity between intervention and disease prevalence, we investigated the in vivo transcriptome of human skin treated with sunscreen and solar-simulated radiation (ssR). A focal skin area of healthy participants was exposed to ssR at 1 minimal erythema dose (MED), 0.1 MED or 100 J/m2 with or without prior application of sunscreen, or to non-UVB-spectrum of ssR (solar-simulated UVA/visible/infrared radiation: ssA). Skin biopsies were analyzed using expression microarrays.

Publication Title

Transcriptional signatures of full-spectrum and non-UVB-spectrum solar irradiation in human skin.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP034736
Overexpression of ERG in cord blood progenitors promotes expansion and recapitulates molecular signatures of high ERG leukemias
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

High expression of the ETS family transcription factor ERG is associated with poor clinical outcome in acute myeloid leukemia (AML) and acute T-cell lymphoblastic leukemia (T-ALL). In murine models, high ERG expression induces both T-ALL and AML. However, no study to date has defined the effect of high ERG expression on primary human hematopoietic cells. In the present study, human CD34+ cells were transduced with retroviral vectors to elevate ERG gene expression to levels detected in high ERG AML. RNA sequencing was performed on purified populations of transduced cells to define the effects of high ERG on gene expression in human CD34+ cells. Integration of the genome-wide expression data with other data sets revealed that high ERG drives an expression signature that shares features of normal hematopoietic stem cells, high ERG AMLs, early T-cell precursor-ALLs and leukemic stem cell signatures associated with poor clinical outcome. Functional assays linked this gene expression profile to enhanced progenitor cell expansion. These results support a model whereby a stem cell gene expression network driven by high ERG in human cells enhances the expansion of the progenitor pool, providing opportunity for the acquisition and propagation of mutations and the development of leukemia. Overall design: RNA sequencing in ERG overexpressing human CD34+ cells

Publication Title

Overexpression of ERG in cord blood progenitors promotes expansion and recapitulates molecular signatures of high ERG leukemias.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE136958
Microarray profiling of in vitro expanded FRCs cultured alone or with activated T cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To investigate whether FRCs express molecules capable of promoting the functions of activated T cells, we expanded FRCs from primary lymph node stromal cell (LNSC) cultures as previously described (Lukacs-Kornek et al., Nature Immunology, 2011), and then cultured them alone or with splenocytes activated with soluble antibody (0.25μg/ml) against CD3 (anti-CD3) and anti-CD28 for 16 hours. FRCs co-cultured with activated T cells upregulated expression of genes encoding molecules known to dampen T cell function such as Arg1, CD274 and Nos2. However, in response to activated T cells, FRCs also upregulated molecules with immunostimulatory capabilities such as Icosl, Cd40 and Il6.

Publication Title

Fibroblastic reticular cells enhance T cell metabolism and survival via epigenetic remodeling.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE18567
Temporal profiling of gene expression in cochleae of wild type and alpha9 null mice
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Efferent inhibition of cochlear outer hair cells is mediated by nicotinic cholinergic receptors containing alpha9 (a9) and alpha10 subunits. Mice lacking a9 nicotinic subunits fail to exhibit classic olivocochlear responses and are characterized by abnormal synaptic morphology at the base of outer hair cells. To detail molecular changes induced upon the loss of a9 subunit, we sampled cochlear RNA from wild type and a9 null mice at postnatal (P) days spanning periods of synapse formation and maturation (P3, P7, P13 and P60). Our findings point to a delay in cochlear maturation starting at the onset of hearing (P13), as well as an up-regulation of various GABA receptor subunits in adult mice lacking the a9 nicotinic subunit.

Publication Title

Lack of nAChR activity depresses cochlear maturation and up-regulates GABA system components: temporal profiling of gene expression in alpha9 null mice.

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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