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accession-icon GSE65939
Both gain and loss of function of miR-126 promote t(8;21) leukemia progression with different consequences and through different mechanisms
  • organism-icon Mus musculus
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

To investigate the pathological effect of miR-126 on the progression of acute myeloid leukemia (AML) induced by AML1-ETO9a (AE9a), we conducted a series of mouse bone marrow transplantation (BMT) assays with the following groups: AE9a (primary donor cells were wild-type mouse bone marrow progenitor (i.e., lineage negative; Lin-) cells retrovirally transduced with MSCV-PIG-AE9a), AE9a+miR-126 (primary donor cells were wild-type mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG-AE9a-miR-126), and miR-126KO+AE9a (primary donor cells were miR-126 knockout mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG-AE9a), along with a control group (primary donor cells were wild-type mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG empty vector). The control group was only used in the primary and secondary BMT assays, whereas the three leukemic groups including AE9a, AE9a+miR-126 and miR-126KO+AE9a were used in four passages (i.e., primary, secondary, tertiary and quaternary) of BMT assays. Then, gene expression profiling was conducted with bone marrow samples collected from different groups to decipher the molecular mechanisms underlying miR-126 effects on leukemia initiation and progression and maintenance and self-renewal of leukemia stem/initiating cells.

Publication Title

Overexpression and knockout of miR-126 both promote leukemogenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE31879
Alterations of methylome and transcriptome in human melanoma: the inverse relationship between epigenome integrity and BRAF mutation
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Melanoma is the deadliest form of skin cancer with rising incidence and mortality rates. Oncogenic mutation in BRAF gene is the single most frequent genetic alteration in human melanoma; however, this event per se is not sufficient to produce melanoma in vivo. We have investigated whether epigenetic changes, specifically aberrant DNA methylation and dysregulation of gene expression, alone or in combination with this genetic event, are involved in the genesis of human melanoma. We have constructed the whole of primary human melanomas in relation to their BRAF mutational status. Our methylation profiling identified a large number of hyper- or hypomethylated genes in melanoma tumors, many of which being novel and having the potential to serve as biomarkers. Gene ontology analysis revealed that gene categories involved in neuronal cell morphology and development, and skin and neurological disorders were highly enriched. Frequently methylated targets included developmental regulatory transcription factors and homeobox genes, which are mostly subjected to bivalent histone marking and Polycomb occupancy in embryonic stem cells. Notably, several genes involved in the MEK-ERK and the PI3K pathways, two of the most frequently perturbed pathways in human melanoma, showed extensive methylation changes. Gene expression profiling identified a long list of dysregulated genes, many of which being involved in melanocytes development and differentiation, and showing concomitant aberrant DNA methylation. Sub-typing of the melanoma tumors based on BRAF mutational status revealed that tumors with a mutated BRAF had distinctive and more pronounced changes in both DNA methylation and gene expression profiles than tumors carrying the wildtype BRAF. The differentially compromised methylome and transcriptome of melanomas (dependent on BRAF mutation) deserves special attention because many epigenetic alterations, including DNA methylation-mediated regulation of gene expression, are potentially reversible. The dichotomous integrity of epigenome in human melanoma holds great promise for the field of personalized medicine.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE40904
Gene expression analysis for Il13Ra2-positive and IL13Ra2-negative glioma cell lines
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Affymetrix expression profiling was used to evaluate the association between IL13R2 expression, and mesenchymal, proneural, classical and neural signature genes expression for glioma subclasses defined by Verhaak et al (Cancer Cell; 2010).

Publication Title

Glioma IL13Rα2 is associated with mesenchymal signature gene expression and poor patient prognosis.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE36403
Profiles of Epigenetic Histone Post-translational Modifications at Type 1 Diabetes Susceptible Genes
  • organism-icon Homo sapiens
  • sample-icon 4 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

Profiles of epigenetic histone post-translational modifications at type 1 diabetes susceptible genes.

Sample Metadata Fields

Specimen part, Disease, Cell line

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accession-icon GSE68643
PBX3 cooperates with MEISI in causing rapid acute myeloid leukemia and recapitulates the core transcriptome of MLL-rearranged leukemia
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

To investigate whether co-expression of PBX3/MEIS1 can mimic that of MLL-AF9, HOXA9/MEIS1 or HOXA9/PBX3 in inducing leukemogenesis, we conducted in vivo mouse bone marrow transplantation (BMT) assays. Briefly, normal mouse bone marrow (BM) progenitor (i.e., lineage negative; Lin-) cells collected from B6.SJL (CD45.1) donor mice (CD45.1) were retrovirally co-transduced with MSCVneo-MLL-AF9+MSCV-PIG (MLL-AF9), MSCVneo-HOXA9+MSCV-PIG (HOXA9), MSCVneo-HOXA9+MSCV-PIG-MEIS1 (HOXA9+MEIS1), MSCVneo-HOXA9+MSCV-PIG-PBX3 (HOXA9+PBX3), MSCV-PIG-PBX3+MSCVneo-MEIS1 (PBX3+MEIS1), MSCVneo+MSCV-PIG-PBX3 (PBX3) , MSCVneo+MSCV-PIG-MEIS1 (MEIS1), or MSCVneo+MSCV-PIG (normal control; NC). Retrovirally transduced cells then were cultured with cytokines as well as puromycin and G418. Seven days later, the donor cells were transplanted into lethally irradiated (960 rads) 8- to 10-week-old C57BL/6 (CD45.2) recipient mice. The transplanted mice were watched for leukemogenesis. Then, gene expression profiling was conducted with bone marrow samples collected from leukemia groups and control group.

Publication Title

PBX3 and MEIS1 Cooperate in Hematopoietic Cells to Drive Acute Myeloid Leukemias Characterized by a Core Transcriptome of the MLL-Rearranged Disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE36509
Identification of differentially expressed genes in LBH589-treated cells
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To identify the targets of LBH589 treatment, we compared gene expression profiles in three different types of human cancer cell lines (H295R, HeLa and MCF-7her2) with and without LBH589 treatment. Affymetrix microarray analysis was performed to determine changes in gene expression that are unique to LBH treatment.

Publication Title

Inhibition of the proliferation of acquired aromatase inhibitor-resistant breast cancer cells by histone deacetylase inhibitor LBH589 (panobinostat).

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE2225
Letrozole-, Anastrozole- and Tamoxifen-Responsive Genes in MCF-7aro Cells
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Anti-estrogens and aromatase inhibitors are important drugs in the treatment of estrogen-dependent breast cancer. In order to investigate the effects of these drugs on gene expression in breast cancer cells, we treated estrogen receptor-positive MCF-7 cells, stably transfected with the aromatase gene (known as MCF-7aro cells), with testosterone, 17-estradiol, two aromatase inhibitors (letrozole and anastrozole), and an anti-estrogen (tamoxifen). Microarray analyses using Affymetrix Human Genome U133A GeneChips were carried out using total RNA isolated from the control and treated cells. When comparing the effect of each inhibitor on gene expression we observe that letrozole and anastrozole are more similar in terms of the genes they affect, compared to treatment with tamoxifen. The results of this study provide us with a better understanding of the actions of both aromatase inhibitors and anti-estrogens at the molecular level. We believe that the results of this study serve as the first step in identifying unique expression patterns following drug treatment, and that this will ultimately be useful in customizing patient treatment strategies for estrogen-dependent breast cancer.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE42310
COHCAP: City of Hope CpG Island Analysis Pipeline
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

COHCAP (City of Hope CpG Island Analysis Pipeline) is an algorithm to analyze single-nucleotide resolution DNA methylation data. It provides QC metrics, differential methylation for CpG Sites, differential methylation for CpG Islands, integration with gene expression data, and visualization of methylation values. COHCAP is currently the only DNA methylation package that can handle integration with gene expression data, and the results of this study show that COHCAP can identify regions of differential methylation with ~50% concordance with gene expression. COHCAP is scalable for analysis of both cell line data and heterogeneous patient data, and it can identify known cancer biomarkers as well as intriguing new roles of epigenetic regulation in cancer (such as methylation of estrogen receptor in breast cancer patients). This study also uses cell line data to show that COHCAP is capable of analyzing Illumina methylation array and targeted bisulfite sequencing data, with either 1-group or 2-group study designs. The accuracy of COHCAP is accessed using qPCR, EpiTect, and comparison of COHCAP regions of differential methylation with MIRA peaks. This software is freely available at https://sourceforge.net/projects/cohcap/.

Publication Title

COHCAP: an integrative genomic pipeline for single-nucleotide resolution DNA methylation analysis.

Sample Metadata Fields

Disease, Cell line

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accession-icon GSE35627
Expression data from Angiotensin II (Ang II)-treated Rat Vascular Smooth Muscle Cells (RVSMC)
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Angiotensin II (Ang II)-mediated vascular smooth muscle cells (VSMC) dysfunction plays a critical role in cardiovascular diseases. However, the gene expression in this process is unclear.

Publication Title

Small RNA sequencing reveals microRNAs that modulate angiotensin II effects in vascular smooth muscle cells.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE99514
Suppression of lung cancer development by aspirin and triptolide
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Chronic inflammation plays important role in lung cancer development. Recently, we found that anti-inflammation drugs aspirin and triptolide when combined showed synergistic effect in suppressing lung cancer development. In this study, we aim to use gene microarray to define the genes and pathways that are affected by aspirin, triptolide individually or in combination.

Publication Title

No associated publication

Sample Metadata Fields

Treatment

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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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