Fig. 3
Validation of mutation status in organoids and parental tumors by Sanger sequencing. (A) The KP model show a double-mutant with confirmed presence of the KrasG12V and Trp53∆ex2−10 mutations in both tumor and organoid samples of KP model. (B) The KPC model shows a triple-mutant with confirmed presence of the KrasG12V, Trp53∆ex2−10 and Ctnnb1∆ex3 mutations in both tumor and organoid samples. Healthy tissue was included as a control and yielded products for the Kras and Ctnnb1 amplicons