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Expression data from mouse intestinal organoids II

ABSTRACT: APC inactivation is the early process in the tumorigenesis of colorectal cancer. We established organoid cultures from intestines of genetically modifeid mice harboring Apcfl/fl, Tacc3wt/wt or Apcfl/fl, Tacc3fl/fll and R26CreERT2 allele We used microarrays to determine the alterations in intestinal stem cells in response to Tacc3 disruption.

ORGANISM(S): Mus musculus

PROVIDER: GSE76848 | GEO | 2016/04/30

SECONDARY ACCESSION(S): PRJNA308751

REPOSITORIES: GEO

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Expression data from mouse intestinal organoids I

2016-03-31 | GSE76847 | GEO

Expression data from mouse intestinal organoids I

Project description:APC inactivation is the early process in the tumorigenesis of colorectal cancer. We established organoid cultures from intestines of genetically modifeid mice harboring Apcfl/fl and R26CreERT2 allele We used microarrays to determine the alterations in intestinal stem cells in response to APC inactivation. Organoids were treated with 4OHT to induce recombination of APC or left untreated, and collected at 4 or 6 days after treatment. RNA were extracted and hybridization on Affymetrix microarrays.

2016-03-31 | E-GEOD-76847 | biostudies-arrayexpress

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Characterization of gastric tumor organoids with specific oncogenic pathway activations

Project description:Gastric cancer ranks the fifth most common malignancy and the third leading cause of cancer related death worldwide. Classical chemotherapy is still the standard treatment in advanced stages, with only two targeted therapies currently in clinical use. Several targeted trials have failed, likely due to missing relevant biomarkers that predict response. Patient derived cancer organoids (PDOs) constitute a three dimensional cell culture system showing self renewal, self organization and regularly unlimited proliferation while faithfully recapitulating many aspects of the tumor they are derived from. Nevertheless, the complex individual mutational landscape hampers the use of PDOs for basic and translational research. We therefore characterized three murine tumor organoid models with defined mutational patterns altering specific oncogenic pathways: a RAS activated (KrasG12D, Tp53R172H), a WNT activated (Apcfl/fl, Tp53R172H) and a diffuse (Cdh1fl/fl, Apcfl/fl) tumor model. The models were analyzed phenotypically, a proteome signature was established and a drug screen performed. The models were morphologically diverse, were characterized by individual protein expression signatures and showed differential drug sensitivities. The developed organoid models allow functional assays as well as pathway specific drug interference testing in a genetically defined setting.

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Gene expression profiels from organoids.

Project description:Recent studies have suggested increased plasticity of differentiated cells within the intestine to act both as intestinal stem cells and tumour initiating cells. However, little is known of the processes that regulate this plasticity. Our previous work has shown that activating mutations of Kras or the NF-kB pathway can drive dedifferentiation of intestinal cells lacking Apc. To investigate this process further, we profiled organoids by gene expression analysis. Organoids were isolated from VillinCreER Apcfl/fl KrasG12D crypts (here called CC) or Villi (here called SFV).

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