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. 2018 Apr 27;68(2):207–217. doi: 10.1136/gutjnl-2017-314549

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Tumour modelling using corpus mouse organoids simulating the chromosomal instable (CIN) and genomic stable (GS) subtype of stomach cancer. (A–H) Established tumour organoids were analysed concerning mutated pathways and compared with normal organoids. (A–B, E–F) Representative pictures of organoids showed differences in morphology. CIN tumours showed smooth layered epithelium compared with normal organoids. GS-WNT tumour organoids had a grape-like structure. (C, G) Immunohistochemistry of normal versus tumour organoids. CIN organoids showed a Tp53 accumulation in the nucleus. GS-WNT organoids showed β-catenin accumulation in the nucleus whereas normal organoids showed membranous expression. (D) Kras pathway of CIN organoids was quantified by Western blot. Tumour organoids were increased in Erk1/2 phosphorylation compared with normal organoids. (H) Quantitative RT-PCR experiments of GS-Wnt organoids. Tumours showed an increased Wnt signalling as measured by Axin2 and Cyclin D1 expression levels compared with normal organoids. Treatment with 5 mM calphostin C decreased pathway activity (scale bar A–G 100 µm, Student’s t-test treated vs non-treated *<0.05; ** < 0.01). (I) Media component release. Each indicated medium component was omitted from the whole medium one by one and organoids passaged two times per week in a 1:2 ratio. (J) Single cell plating of organoids. One hundred single cells were plated per well and originating organoids counted after 7 days. Student’s t-test tumour versus control (*<0.05).