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accession-icon GSE24006
A Leukemic Stem Cell Expression Signature is Associated with Clinical Outcomes in Acute Myeloid Leukemia
  • organism-icon Homo sapiens
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Context: In many cancers, specific subpopulations of cells appear to be uniquely capable of initiating and maintaining tumors. The strongest support for this cancer stem cell model comes from transplantation assays in immune-deficient mice indicating that human acute myeloid leukemia (AML) is organized as a cellular hierarchy driven by self-renewing leukemia stem cells (LSC). This model has significant implications for the development of novel therapies, but its clinical significance remains unclear.

Publication Title

Association of a leukemic stem cell gene expression signature with clinical outcomes in acute myeloid leukemia.

Sample Metadata Fields

Disease, Disease stage, Subject

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accession-icon GSE38816
Intratumoral diversity in Follicular lymphoma
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Follicular lymphoma (FL) shows heterogenous expression of the cell surface B-cell marker, CD20. In order to investigate whether this heterogeneity also marks underlying transcriptional heterogeneity, we sorted tumor B-cells from 8 FL specimens based upon their intermediate or high expression of CD20 and transcriptionally profiled them.

Publication Title

Hierarchy in somatic mutations arising during genomic evolution and progression of follicular lymphoma.

Sample Metadata Fields

Sex, Age, Subject

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accession-icon GSE48397
Expression data from (mouse) normal lung fibroblasts and carcinoma-associated fibroblasts
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Cancer-associated fibroblasts (CAFs) have been reported to support tumor progression by a variety of mechanisms. However, their role in the progression of non-small cell lung cancer (NSCLC) remains poorly defined. In addition, the extent to which specific proteins secreted by CAFs contribute directly to tumor growth is unclear. To study the role of CAFs in NSCLC, a cross-species functional characterization of mouse and human lung CAFs was performed, including gene expression analysis comparing normal mouse lung fibroblasts (NFs) and mouse lung CAFs to seek for differentially-expressed secreted proteins.

Publication Title

Cross-species functional analysis of cancer-associated fibroblasts identifies a critical role for CLCF1 and IL-6 in non-small cell lung cancer in vivo.

Sample Metadata Fields

Specimen part

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accession-icon SRP108846
Bulk cell RNAseq of putatative intestinal stem cell populations
  • organism-icon Mus musculus
  • sample-icon 82 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

A comparative bulk cell RNA-seq analysis of diverse intestinal stem cell populations was performed, for cells expressing the following markers: Lgr5-eGFPhi, Cd166+, Cd24lo, Grp78, upper side population (SP), Bmi1, mTert, Hopx, Dclk1, a lower side population (SP) Overall design: For each ISC population of interest, three independent mice (biological replicates) were used. From each mouse, a marker-“positive” and a marker-“negative” population were collected, as well as a "total" population.

Publication Title

Intestinal Enteroendocrine Lineage Cells Possess Homeostatic and Injury-Inducible Stem Cell Activity.

Sample Metadata Fields

Disease, Subject

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accession-icon GSE10377
Strains for eQTL CNV Analysis
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Background

Publication Title

Expression quantitative trait loci mapping identifies new genetic models of glutathione S-transferase variation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE21061
Endogenous overexpression of Poplar MYB186 increases trichome density, improves growth rate and insect pest resistance
  • organism-icon Populus tremula x populus alba
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Poplar Genome Array (poplar)

Description

Trichomes are specialised epidermal cells that generally play a role in reducing transpiration and act as a deterrent to herbivory. In a screen of activation tagged Populus tremula x P. alba 717-1B4 trees, we identified a mutant line, fuzzy, with increased foliar trichome density. This mutant also had a 35% increase in growth rate and a 200% increase in the rate of photosynthesis as compared to wild-type poplar. The fuzzy mutant had significant resistance to feeding by larvae of the white spotted tussock moth (Orgyia leucostigma), a generalist insect pest of poplar trees. The fuzzy phenotype is attributable to activation tagging and increased expression of the gene encoding PtaMYB186, which is related to Arabidopsis thaliana MYB106, a known regulator of trichome initiation. The fuzzy phenotype can be recapitulated by overexpressing PtaMYB186 in poplar. PtaMYB186 overexpression results in reconfiguration of the poplar transcriptome, with changes in the transcript abundance of suites of genes that are related to trichome differentiation. It is notable that this gene responsible for trichome development also altered traits related to growth rate and pest resistance, suggesting that non-intuitive facets of plant development might be useful targets for plant improvement.

Publication Title

Endogenous overexpression of Populus MYB186 increases trichome density, improves insect pest resistance, and impacts plant growth.

Sample Metadata Fields

Specimen part

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accession-icon GSE6476
Effect of chronic fluoxetine treatment on hippocampal gene expression
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Both the mechanism of action and the factors determining the behavioral response to antidepressants are unknown. It has been shown that antidepressant treatment promotes the proliferation and survival of hippocampal neurons via enhanced serotonergic signaling, but it is still unclear whether hippocampal neurogenesis is responsible for the behavioral response to antidepressants. Furthermore, a large subpopulation of patients fails to respond to antidepressant treatment due to presumed underlying genetic factors. In the present study, we have used the phenotypic and genotypic variability of inbred mouse strains to show that there is a genetic component to both the behavioral and neurogenic effects of chronic fluoxetine treatment, and that this antidepressant induces an increase in hippocampal cell proliferation only in the strains that also show a positive behavioral response to treatment. The behavioral and neurogenic responses are associated with an upregulation of genes known to promote neuronal proliferation and survival. These results suggest that inherent genetic predisposition to increased serotonin-induced neurogenesis is a determinant of antidepressant efficacy.

Publication Title

Genetic regulation of behavioral and neuronal responses to fluoxetine.

Sample Metadata Fields

Sex, Treatment

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accession-icon SRP011185
RAMPAGE dataset for the human K562 cell line
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

5''-complete cDNA sequencing on ribosome-depleted total RNA from the human K562 cell line. Provides high-quality, genome-wide single-base resolution profiling of transcription start sites and their expression levels. Overall design: This dataset represents a whole-genome, single-base resolution profiling of transcription start site (TSS) expression in the human K562 cell line. These profiles were established using RAMPAGE, a high-throughput, high-accuracy 5''-complete cDNA sequencing method implemented on the Illumina platform. The data was analyzed using custom scripts and algorithms that are all available upon request.

Publication Title

High-fidelity promoter profiling reveals widespread alternative promoter usage and transposon-driven developmental gene expression.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE47150
Microarray profiling of primary neurons transduced with shRNA for multiple ASD-implicated genes
  • organism-icon Mus musculus
  • sample-icon 37 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Austism spectrum disorder (ASD) is a heterogeneous behavioral disease most commonly characterized by severe impairment of social engagement and the presence of repetitive activities. The molecular etiology of ASD is still largely unknown despite a strong genetic component. Part of the difficulty in turning genetics into disease mechanisms and potentially new therapeutics is the sheer number and diversity of the genes that have been associated with ASD and ASD symptoms. The goal of this work is to use shRNA-generated models of genetic defects proposed as causative for ASD to identify the common pathways that might explain how they produce a common clinical outcome. Transcript levels of Mecp2, Mef2a, Mef2d, Fmr1, Nlgn1, Nlgn3, Pten, and Shank3 were knocked-down in mouse primary neuron cultures using shRNA/lentivirus constructs. Whole genome expression analysis was conducted for each of the knock-down cultures as well as a mock-transduced culture and a culture exposed to a lentivirus expressing luciferase. Gene set enrichment and a causal reasoning engine were employed to indentify pathway level perturbations generated by the transcript knock-down. Quantitation of the shRNA targets confirmed the successful knock-down at the transcript and protein levels of at least 75% for each of the genes. After subtracting out potential artifacts caused by transfection and viral infection, gene set enrichment and causal reasoning engine analysis showed that a significant number of gene expression changes mapped to pathways associated with neurogenesis, long-term potentiation, and synaptic activity. This work demonstrates that despite the complex genetic nature of ASD, there are common molecular mechanisms that connect many of the best established autism candidate genes. By identifying the key regulatory checkpoints in the interlinking transcriptional networks underlying autism, we are better able to discover the ideal points of intervention that provide the broadest efficacy across the diverse population of autism patients.

Publication Title

Transcriptomic analysis of genetically defined autism candidate genes reveals common mechanisms of action.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE16744
Wild-type and COUP-TFI-/- newborn inner ear microarrays
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

In order to establish a list of candidate direct COUP-TFI gene targets in the inner ear, we analyzed the differential gene expression profiles of the wild-type and the COUP-TFI/ P0 inner ears.

Publication Title

Genome-wide analysis of binding sites and direct target genes of the orphan nuclear receptor NR2F1/COUP-TFI.

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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