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accession-icon GSE75415
Gene exrpression profiling of childhood adrenocortical tumors
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Pediatric adrenocortical tumors (ACT) are rare and often fatal malignancies; little is known regarding their etiology and biology. To provide additional insight into the nature of ACT, we determined the gene expression profiles of 24 pediatric tumors (five adenomas, 18 carcinomas, and one undetermined) and seven normal adrenal glands. Distinct patterns of gene expression, validated by quantitative real-time PCR and Western blot analysis, were identified that distinguish normal adrenal cortex from tumor. Differences in gene expression were also identified between adrenocortical adenomas and carcinomas. In addition, pediatric adrenocortical carcinomas were found to share similar patterns of gene expression when compared with those published for adult ACT. This study represents the first microarray analysis of childhood ACT. Our findings lay the groundwork for establishing gene expression profiles that may aid in the diagnosis and prognosis of pediatric ACT, and in the identification of signaling pathways that contribute to this disease.

Publication Title

Gene expression profiling of childhood adrenocortical tumors.

Sample Metadata Fields

Sex

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accession-icon SRP043960
GATA2 shRNA Expression in Castration Resistant Prostate Cancer Cell Lines
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

The transcription factor GATA2 regulates chemotherapy resistance in prostate cancer. We report a novel GATA2 transcriptional program that has implications for chemotherapy resistance disease and aggressiveness in castration resistant prostate cancer. Overall design: Examination of the transcriptional network changes induced in human Ch-CRPC cell lines by two shRNA mediated knock down of GATA2 versus random shRNA control

Publication Title

A targetable GATA2-IGF2 axis confers aggressiveness in lethal prostate cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE54582
Transcriptomic analysis of mammary tumors from MMTV-ErbB2 transgenic mice
  • organism-icon Mus musculus
  • sample-icon 222 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The tyrosine kinase ErbB2 positive breast tumors have more aggressive tumor growth, poorer clinical outcome, and more resistance to radiotherapy, chemotherapy and hormone therapy. A humanized anti-ErbB2 monoclonal antibody Herceptin and a small molecules inhibitor Lapatinib were developed and approved by FDA to treat patients with ErbB2 amplification and overexpression. Unfortunately, most ErbB2+ breast cancers do not respond to Herceptin and Lapatinib, and the majority of responders become resistant within 12 months of initial therapy (defined as secondary drug resistance). Such differences in response to Lapatinib treatment is contributed by substantial heterogeneity within ErbB2+ breast cancers. To address this possibility, we carried out transcriptomic analysis of mammary tumors from genetically diverse MMTV-ErbB2 mice. This will help us to have a better understanding of the heterogeneous response to ErbB2 targeted therapy and permit us to design better and more individualized (personalized) treatment strategies for human ErbB2 positive breast cancer.

Publication Title

Unraveling heterogeneous susceptibility and the evolution of breast cancer using a systems biology approach.

Sample Metadata Fields

Specimen part

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accession-icon GSE109284
LXR nuclear receptors are transcriptional regulators of dendritic cell chemotaxis
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The liver X receptors (LXRs) are ligand-activated nuclear receptors with established roles in the maintenance of lipid homeostasis in multiple tissues. LXRs exert additional biological functions as negative regulators of inflammation, particularly in macrophages. However, the transcriptional responses controlled by LXRs in other myeloid cells, such as dendritic cells (DC), are still poorly understood. Here we used gain- and loss-of-function models to characterize the impact of LXR deficiency on DC activation programs. Our results identified an LXR-dependent pathway that is important for DC chemotaxis. LXR-deficient mature DCs are defective in stimulus-induced migration in vitro and in vivo. Mechanistically, we show that LXRs facilitate DC chemotactic signaling by regulating the expression of CD38, an ectoenzyme important for leukocyte trafficking. Pharmacological or genetic inactivation of CD38 activity abolished LXR-dependent induction of DC chemotaxis. Using the LDLR-/- mouse model of atherosclerosis, we also demonstrated that hematopoietic CD38 expression is important for the accumulation of lipid-laden myeloid cells in lesions, suggesting that CD38 is a key factor in leukocyte migration during atherogenesis. Collectively, our results demonstrate that LXRs are required for efficient emigration of DCs in response to chemotactic signals during inflammation.

Publication Title

LXR nuclear receptors are transcriptional regulators of dendritic cell chemotaxis.

Sample Metadata Fields

Specimen part

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accession-icon GSE109277
Gene expression profile of in vitro differentiated mouse bone marrow-derived dendritic cells.
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Mouse BMDCs were differentiated from bone marrow by GM-CSF and IL-4 for 9 days.

Publication Title

LXR nuclear receptors are transcriptional regulators of dendritic cell chemotaxis.

Sample Metadata Fields

Specimen part

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accession-icon GSE56741
Gene expression profile of collagen VI deficient human fibroblasts
  • organism-icon Homo sapiens
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

In order to gain insight into the molecular pathogenesis of collagen VI defects we have performed gene expression microarray analysis of dermal fibroblasts. We have compared the transcriptome of fibroblasts, treated or untreated with ascorbic acid, from UCMD patients (n = 6) and aged-matched healthy children (n = 5).

Publication Title

Transcriptome Analysis of Ullrich Congenital Muscular Dystrophy Fibroblasts Reveals a Disease Extracellular Matrix Signature and Key Molecular Regulators.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Treatment

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accession-icon GSE48805
Comparison of gene expression profile in RAG2+ B lineage cells from the small intestinal lamina propria and RAG2+ B lineage cells from the bone marrow
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We used a RAG2-GFP reporter mouse to show that RAG+ B lineage cells can be found in the small intestinal lamina proria in normally-housed mice at weaning age. We used microarry expression analysis to compare the RAG2+ population in the gut to the RAG2+ B lineage population in the bone marrow.

Publication Title

Microbial colonization influences early B-lineage development in the gut lamina propria.

Sample Metadata Fields

Specimen part

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accession-icon GSE18732
mRNA expression data from skeletal muscle of type 2 diabetes
  • organism-icon Homo sapiens
  • sample-icon 117 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarray technology to profile mRNA expression in the skeletal muscle of normal (NGT), glucose intolerant (IGT) and type 2 diabetic (DM) subjects. Groups were classified using WHO criteria and, importantly, the DM group were free of anti hypoglycaemic medication for one week prior to biopsy.

Publication Title

Integration of microRNA changes in vivo identifies novel molecular features of muscle insulin resistance in type 2 diabetes.

Sample Metadata Fields

Sex, Age

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accession-icon SRP091435
Adaptive chromatin remodeling in glioblastoma stem cell plasticity and drug tolerance
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

Many cancers are postulated to harbor developmental hierarchies in which cells display variability in stem-like character, tumor propagating ability, and proliferation. In glioblastoma (GBM), glioma stem cells (GSCs) reside atop such a tumor cellular hierarchy, and are thought to resist current therapies and thus underlie inevitable relapse. Here we show that GSCs can evade RTK inhibition by reversibly regressing to a slow-cycling state reminiscent of quiescent neural stem cells. This process involves up-regulation of numerous histone demethylases, including KDM6A/B, which remodel the chromatin landscape and are selectively essential for drug persister survival. Chromatin remodeling is accompanied by activation of various neurodevelopmental master regulators and Notch signaling, changes which closely parallel critical aspects of neural stem cell biology. Thus our findings illustrate how cancer cells may hijack native developmental programs for deranged proliferation, adaptation, and tolerance in the face of stress. Our studies highlight key roles for chromatin remodeling and developmental plasticity in GBM biology, and suggest strategies for overcoming therapeutic resistance by targeting epigenetic and developmental pathways. Overall design: ChIP-seq for histone modifications and Notch factors in glioblastoma stem cell lines with various drug treatments RNA-seq in glioblastoma stem cell lines with various drug treatments

Publication Title

Adaptive Chromatin Remodeling Drives Glioblastoma Stem Cell Plasticity and Drug Tolerance.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE30407
The ets transcription factor ELF5 suppresses the estrogen sensitive phenotype and contributes to antiestrogen resistance in luminal breast cancer.
  • organism-icon Homo sapiens
  • sample-icon 14 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

ELF5 suppresses estrogen sensitivity and underpins the acquisition of antiestrogen resistance in luminal breast cancer.

Sample Metadata Fields

Cell line, Treatment, Time

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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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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