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accession-icon GSE64566
GE/miRNA expression profile of Human Epicardial Adipose Tissue (EAT) and Subcutaneous Adipose Tissue (SAT) in Patients with Coronary Artery Disease (CAD) vs. Controls (CTRL)
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrative miRNA and whole-genome analyses of epicardial adipose tissue in patients with coronary atherosclerosis.

Alternate Accession IDs

E-GEOD-64566

Sample Metadata Fields

Age, Specimen part, Disease, Disease stage

View Samples
accession-icon GSE64554
GE/miRNA expression profile of Human Epicardial Adipose Tissue (EAT) and Subcutaneous Adipose Tissue (SAT) in Patients with Coronary Artery Disease (CAD) vs. Controls (CTRL) - PART 1 - Genes
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

Gene expression profiles of Human EAT vs. SAT (CTRL & CAD). The aim of the present study was to assess a gene expression chart characterizing EAT vs. SAT, and CAD vs. CTRL. Results provide the information that EAT is characterized by a differential expression of different genes when compared to its reference tissue (SAT), and that EAT is characterized by specific gene expression changes in patients with CAD.

Publication Title

Integrative miRNA and whole-genome analyses of epicardial adipose tissue in patients with coronary atherosclerosis.

Alternate Accession IDs

E-GEOD-64554

Sample Metadata Fields

Age, Specimen part, Disease, Disease stage

View Samples
accession-icon GSE974
Left ventricular apex samples
  • organism-icon Homo sapiens
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

19 paired human left ventricular apex samples were harvested at the time of implant of a left ventricular assist device (PRE) and at the time of explant (POST). The cohort included patients that were clinically classified as "ischemic" (I) showing evidence of coronary artery disease, "non-ischemic" (N) no evidence of coronary artery disease or "acute Myocardial infarction" (IM) myocardial infarction within 10 days of the implant. Tissue was processed and hybridized to the Affymetrix HG-U133A chip.

Publication Title

Genomic profiling of the human heart before and after mechanical support with a ventricular assist device reveals alterations in vascular signaling networks.

Alternate Accession IDs

E-GEOD-974

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP094498
Systemic human ILC precursors provide a substrate for tissue ILC differentiation
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Innate lymphoid cells (ILC) represent innate versions of T helper and cytotoxic T cells that differentiate from committed ILC precursors (ILCP). Still, how ILCP relate to mature tissue-resident ILCs remains unclear. We observed that a population of CD117+ ILC from peripheral blood (PB) of healthy donors does not represent any conical ILC subset, but expressed marker (CD117) commonly expressed by hemato-lymphoid progenitors. We therefore hypothesized PB CD117+ ILC might include uncommitted lymphoid precursors. In order to further understand the identity of PB CD117+ ILC, we profiled the transcriptome of highly purified circulating CD117+ ILC compared to CD34+ HSC, the latter representing immature hematopoietic progenitors with multi-lineage potential. Clear differences in gene expression profiles emerged, with a large cluster of 1540 genes expressed at substantially higher levels in CD117+ ILC. In contrast, CD34+ HSC cells highly expressed genes involved in the broad development of diverse hematopoietic lineages. Compared to HSC, CD117+ ILC express high levels of TF that have been shown to be essential for murine ILC development and we did not detect transcripts characteristic of T and B cells development. Transcriptomic analysis suggested that CD117+ ILC represent lymphoid-biased progenitors carrying a TF expression profile resembling a multi-potent ILC precursor (ILCP). Overall design: CD117+ ILC and CD34+ HSC were freshly isolated by FACS of peripheral blood of two healthy adult individuals. In total, 4 samples were analyzed and comparing between two cell populations.

Publication Title

Systemic Human ILC Precursors Provide a Substrate for Tissue ILC Differentiation.

Alternate Accession IDs

GSE90834

Sample Metadata Fields

Specimen part, Disease, Disease stage, Treatment, Subject

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accession-icon GSE101323
An actionable pathway connecting NFATc2 to FOXM1 and EZH2 controls the MITFlo/invasive melanoma phenotype
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Dissection of melanoma heterogeneity through gene expression profiling has led to the identification of two major phenotypes, conventionally defined as MITF high / proliferative and AXL high / invasive. Tumors or single melanoma cells characterized by a predominant AXL-related gene program show enhanced expression of sets of genes involved in motility, invasion and regulation of epithelial-mesenchymal transition (EMT), while these genes are downregulated in tumors or cells with a predominant MITF-related gene program. The activation of the AXLhi/MITFlo invasive gene program in melanoma is characterized by aberrant expression of transcription factors (TFs) involved in the embryonic EMT process. Additional master genes involved in promoting melanoma growth and invasive state have been identified within the family of epigenetic regulators. Two of these genes, RNF2 and EZH2, components of the polycomb repressive complexes 1 and 2, act by epigenetically silencing tumor suppressors that in turn regulate the invasive and EMT-like phenotype of melanoma cells. Additional master genes involved in promoting melanoma growth and invasive state have been identified within the family of epigenetic regulators. Two of these genes, RNF2 and EZH2, components of the polycomb repressive complexes 1 and 2, act by epigenetically silencing tumor suppressors that in turn regulate the invasive and EMT-like phenotype of melanoma cells. Here we provide evidence for a new actionable pathway that controls melanoma EMT-like/invasive phenotype. We show that in MITFlo melanomas, the TF NFATc2 controls the EMT-like transcriptional program, the invasive ability of neoplastic cells, as well as in-vitro and in-vivo growth, through a pathway that functionally links c-myc to FOXM1 and EZH2. Targeting of NFATc2, FOXM1 or EZH2 inhibited melanoma migratory and invasive activity. Moreover, pharmacological co-targeting of NFATc2 and EZH2 promoted apoptosis of BRAF-mutant melanomas with intrinsic resistance to BRAF inhibition.

Publication Title

An actionable axis linking NFATc2 to EZH2 controls the EMT-like program of melanoma cells.

Alternate Accession IDs

E-GEOD-101323

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE59882
Combinatorial treatments targeting MAPK and PI3K/mTOR pathways in metastatic melanoma
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Therapeutic targeting of BRAFV600E has shown a significant impact on progression-free and overall survival in advanced melanoma, but only a fraction of patients benefit from these treatments, suggesting that additional signaling pathways involved in melanoma growth/survival need to be identified. In fact MAPK and PI3K/mTOR signaling pathways are constituively activated in most cancers, including melanoma, to sustain the melanoma growth/survival. A large panel of melanoma were characterized for resistance/susceptibility to different inhibitors targeting MAPK and PI3K/mTOR signaling pathways and the synergistic effect of combinatorial treatments affecting both pathways. These effects were evaluated in terms of cell viability (MTT), apoptosis (Annexin V-PI), caspase 3/7 activity and subG1 cell fraction, highlighting a hierarchy in the combination effects. Further, a smaller panel of melanoma cell lines, were treated with inhibitors singularly and in combination to test the effects on the expression of principal proteins involved in these two pathways. Gene expression profile was performed to analyse the gene modulation induced by inhibitors to identify new strategies to fight melanoma resistance.

Publication Title

Primary cross-resistance to BRAFV600E-, MEK1/2- and PI3K/mTOR-specific inhibitors in BRAF-mutant melanoma cells counteracted by dual pathway blockade.

Alternate Accession IDs

E-GEOD-59882

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE48680
Glucocorticoid effect on mRNA translation in childhood acute lymphoblastic leukemia
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [CDF: huex10stv2_67_020 (huex10st)

Description

Glucocorticoids (GCs) are a central component in treating childhood acute lymphoblastic leukemia (chALL). They mainly act via regulating gene transcription. However, control of mRNA translation by GC has never been assessed systematically. In our research, T- and precursor B-ALL cells were cultured with and without GC for 6 hours and subjected to translational profiling, a technique combining sucrose gradient fractionation and microarray analysis of mRNA in different fractions. Analysis of GC regulation in different pools revealed no significant differences in regulation of mRNA translation by GC, suggesting no evidence for translational regulation by GC.

Publication Title

Translational profiling in childhood acute lymphoblastic leukemia: no evidence for glucocorticoid regulation of mRNA translation.

Alternate Accession IDs

E-GEOD-48680

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE107039
Epigenetic and transcriptomic signature of aging in human liver
  • organism-icon Homo sapiens
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Molecular Aging of Human Liver: An Epigenetic/Transcriptomic Signature.

Alternate Accession IDs

E-GEOD-107039

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE107037
Epigenetic and transcriptomic signature of aging in human liver [expression]
  • organism-icon Homo sapiens
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profiling of liver biopsies collected from 33 healthy liver donors ranging from 13 to 90 years old. The Affymetrix HG-U133 Plus 2.0 GeneChip platform was used to evaluate gene-expression.

Publication Title

Molecular Aging of Human Liver: An Epigenetic/Transcriptomic Signature.

Alternate Accession IDs

E-GEOD-107037

Sample Metadata Fields

Sex, Age, Specimen part, Disease

View Samples
accession-icon GSE81948
miR-204 down-regulation elicited perturbation of a gene target signature common to human cholangiocarcinoma and gastric cancer.
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

There is high need of novel diagnostic and prognostic tools for tumors of the digestive system, such as gastric cancer and cholangiocarcinoma.

Publication Title

MiR-204 down-regulation elicited perturbation of a gene target signature common to human cholangiocarcinoma and gastric cancer.

Alternate Accession IDs

E-GEOD-81948

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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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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