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accession-icon GSE33201
A mouse model of the most aggressive subgroup of human medulloblastoma
  • organism-icon Mus musculus
  • sample-icon 64 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A mouse model of the most aggressive subgroup of human medulloblastoma.

Sample Metadata Fields

Specimen part

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accession-icon GSE33199
A mouse model of the most aggressive subgroup of human medulloblastoma [Mouse430_2]
  • organism-icon Mus musculus
  • sample-icon 64 Downloadable Samples
  • Technology Badge Icon

Description

Mouse models of medulloblastoma are compared to human subgroups through microarray expression and other measures

Publication Title

A mouse model of the most aggressive subgroup of human medulloblastoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE21687
Comparative genomics matches mutations and cells to generate faithful ependymoma models
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon

Description

Genomic technologies have unmasked molecularly distinct subgroups among tumors of the same histological type; but understanding the biologic basis of these subgroups has proved difficult since their defining alterations are often numerous, and the cellular origins of most cancers remain unknown. We sought to decipher complex genomic data sets by matching the genetic alterations contained within these, with candidate cells of origin, to generate accurate disease models. Using an integrated genomic analysis we first identified subgroups of human ependymoma: a form of neural tumor that arises throughout the central nervous system (CNS). Validated alterations included amplifications and homozygous deletions of genes not yet implicated in ependymoma. Matching the transcriptomes of human ependymoma subgroups to those of distinct types of mouse radial glia (RG)neural stem cells (NSCs) that we identified previously to be a candidate cell of origin of ependymoma - allowed us to select RG types most likely to represent cells of origin of disease subgroups. The transcriptome of human cerebral ependymomas that amplify EPHB2 and delete INK4A/ARF matched most closely that of embryonic cerebral Ink4a/Arf-/- RG: remarkably, activation of EphB2 signaling in this RG type, but not others, generated highly penetrant ependymomas that modeled accurately the histology and transcriptome of one human cerebral tumor subgroup (subgroup D). Further comparative genomic analysis revealed selective alterations in the copy number and expression of genes that regulate neural differentiation, particularly synaptogenesis, in both mouse and human subgroup D ependymomas; pinpointing this pathway as a previously unknown target of ependymoma tumorigenesis. Our data demonstrate the power of comparative genomics to sift complex genetic data sets to identify key molecular alterations in cancer subgroups.

Publication Title

Cross-species genomics matches driver mutations and cell compartments to model ependymoma.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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accession-icon GSE15796
Spatiotemporal Analysis of Transcriptome in the paraxial mesoderm of zebrafish embryos
  • organism-icon Danio rerio
  • sample-icon 2 Downloadable Samples
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Description

Differentially expressed genes along the paraxial mesoderm of 12 somite stage zebrafish embryos are identified

Publication Title

Spatiotemporal compartmentalization of key physiological processes during muscle precursor differentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE19677
Striatum of Huntington's disease model mice
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Transcriptional changes in Huntington disease identified using genome-wide expression profiling and cross-platform analysis.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE18551
Striatum of Huntington's disease model mice [Affymetrix data]
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon

Description

Evaluation of transcriptional changes in the striatum may be an effective approach to understanding the natural history of changes in expression contributing to the pathogenesis of Huntington disease (HD). We have performed genome-wide expression profiling of the YAC128 transgenic mouse model of HD at 12 and 24 months of age using two platforms in parallel; Affymetrix and Illumina. We performed gene expression profiling on the same striatal mRNA across both platforms.

Publication Title

Transcriptional changes in Huntington disease identified using genome-wide expression profiling and cross-platform analysis.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE17647
Involvement of 4E-BP1 in the protection induced by HDLs on pancreatic beta cells
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon

Description

High-density lipoproteins (HDLs) protect pancreatic cells against apoptosis. This property might be related to the increased risk to develop diabetes in patients with low HDL blood levels. However, the mechanisms by which HDLs protect cells are poorly characterized. Here we use a transcriptomic approach to identify genes differentially modulated by HDLs in cells subjected to apoptotic stimuli.

Publication Title

Involvement of 4E-BP1 in the protection induced by HDLs on pancreatic beta-cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE45229
Unique pharmacological actions of atypical neuroleptic quetiapine: possible role in cell cycle/fate control
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon

Description

Quetiapine is an atypical neuroleptic with a pharmacological profile distinct from classic neuroleptics. It is currently approved for treating patients with schizophrenia, major depression and bipolar I disorder. However, its cellular effects remain elusive.

Publication Title

Unique pharmacological actions of atypical neuroleptic quetiapine: possible role in cell cycle/fate control.

Sample Metadata Fields

Sex, Treatment

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accession-icon GSE32905
EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors in transgenic mice.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE111392
Differentiation analysis of Mouse Posterior Neural tube
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Posterior embryonic axis develops from neuromesodermal progenitors which differentiate into neural tube and paraxial mesoderm

Publication Title

Recapitulating early development of mouse musculoskeletal precursors of the paraxial mesoderm <i>in vitro</i>.

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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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