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accession-icon GSE51927
Expression analysis of murine primary and derived orthotopic SEOC tumors
  • organism-icon Mus musculus
  • sample-icon 58 Downloadable Samples
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Description

We previously generated genetically engineered mouse (GEM) models based on perturbation of Tp53, Rb with or without Brca1 or Brca2 that develop serous epithelial ovarian cancer (SEOC) closely resembling the human disease on histologic and molecular levels. We have adapted these GEM models to orthotopic allografts that uniformly develop tumors with short latency in immunocompetent recipients and are ideally suited for routine preclinical studies. To monitor passaged tumors at the molecular level, we analyzed transcriptional profiles of a set of primary SEOC and matching derived passaged tumors. We have merged this dataset with previously published ( doi: 10.1158/0008-5472.CAN-11-3834; PMID 22617326) dataset of murine primary ovarian tumors from our GEM models (GSE46169) and merged and compared them to expression profiles of human dataset published previously (doi: 10.1038/nature10166).

Publication Title

Pathway-specific engineered mouse allograft models functionally recapitulate human serous epithelial ovarian cancer.

Alternate Accession IDs

E-GEOD-51927

Sample Metadata Fields

Specimen part

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accession-icon GSE26069
Inducible Astrocytomas in Genetically Engineered Mice
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Evolutionary etiology of high-grade astrocytomas.

Alternate Accession IDs

E-GEOD-26069

Sample Metadata Fields

Sex, Time

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accession-icon GSE26002
Inducible Astrocytomas in Genetically Engineered Mice: Affymetrix
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
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Description

To determine the regulatory pathways necessary for astrocytoma formation within complex adult brain microenvironments, we engineered mice for adult astrocyte-specific disruption of key regulators (pRb, Kras and Pten). Drivers of all astrocytoma grades were identified using CreERTM-inducible alleles. Inactivation of pRb was necessary to initiate grade II disease, and was the only lesion to do so. Additional activation of Kras progressed disease to grade III, while further Pten inactivation facilitated grade IV (glioblastoma) progression. These outcomes were elicited whether somatic events were induced broadly or focally. In vivo inactivation of pRb, which induced astrocyte proliferation and apoptosis, activated the MAPK pathway, while Kras activation and Pten loss triggered PI3K pathways.

Publication Title

Evolutionary etiology of high-grade astrocytomas.

Alternate Accession IDs

E-GEOD-26002

Sample Metadata Fields

Sex, Time

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accession-icon GSE85171
Epigenetic Reprogramming of mutant RAS-driven Rhabdomyosarcoma via MEK Inhibition
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 4 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

MEK inhibition induces MYOG and remodels super-enhancers in RAS-driven rhabdomyosarcoma.

Alternate Accession IDs

E-GEOD-85171

Sample Metadata Fields

Treatment, Time

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accession-icon GSE112776
Expression data for High and Low permeable brain metastases in 231-BR mouse model
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 22 Downloadable Samples
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Description

All highly and poorly permeable metastases from the same mouse brain were collected by laser capture microdissection. Total RNA from both metastatic lesions and immediate microenvironment was isolated from 5 mice bearing 231-BR metastases. As control 4 healthy mouse brains were included.

Publication Title

Reactive astrocytic S1P3 signaling modulates the blood-tumor barrier in brain metastases.

Alternate Accession IDs

E-GEOD-112776

Sample Metadata Fields

Subject

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accession-icon GSE85168
Oncogenic RAS blocks myogenic differentiation
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

C2C12 mouse myoblasts expressing RAS mutants identified in human tumors fail to differentiate in low serum media.

Publication Title

MEK inhibition induces MYOG and remodels super-enhancers in RAS-driven rhabdomyosarcoma.

Alternate Accession IDs

E-GEOD-85168

Sample Metadata Fields

No sample metadata fields

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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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