Extended Data Fig. 2. Lgr5-p53^KO cells have a selective advantage in the setting of dietary carcinogen to promote premalignant gastric lesions.

(a) Recombination specific PCR of DNA extract from gastric lesions of Lgr5-p53^WT and Lgr5-p53^KO mice. Data presented as mean ± s.d of three technical replicates.

(b) Schematic showing Lgr5-p53^LSL-R270H experimental design; DCA/MNU treatment and tamoxifen injection schedule during indicated duration depicted below. (c) Kaplan-Meier survival curve of Lgr5-p53^R270H experiments; table shows frequency of dysplasia in DCA/MNU treated mice of indicated genotype.

(d) Schematic showing Lgr5-p53^KO experimental design; DCA alone, MNU alone, or DCA/MNU combination as well as tamoxifen injection schedule during indicated duration depicted below. Table shows frequency of dysplasia in Lgr5-p53^KO mice with indicated treatment after 12 months. *1/6 Cre-negative, tamoxifen-induced control mice treated with DCA/MNU developed dysplasia.