Extended Data Fig. 1: Dietary carcinogen exposure promotes premalignant and malignant gastric lesions. | Nature Genetics

Extended Data Fig. 1: Dietary carcinogen exposure promotes premalignant and malignant gastric lesions.

From: Early TP53 alterations engage environmental exposures to promote gastric premalignancy in an integrative mouse model

Extended Data Fig. 1

a Schematic of the central hypothesis: Chronic inflammation and carcinogen exposure collaborate with early genomic alterations (for example TP53 mutations) to enable the development of premalignant gastric lesions and eventual invasive cancer. b, Schematic of p53WT mice treated with DCA, MNU, or DCA+MNU combination for 18 months. c, Dissection microscope images of lower esophagus and stomach flayed open along greater curvature (top panel) and histopathological H&E staining (bottom panel) of gastric antrum. *A subset of mice died before the endpoint of the experiment due to other carcinogen-induced cancers (e.g. thymomas). Scale bar = 125μM. d, Mutation signature analysis shows C→T changes characteristic of alkylating agent associated Signature 11. center line: median, lower hinge: the first quartile (Q1), upper hinge: the third quartile (Q3), extreme of the lower whisker: Q1 – 1.58 * (Q3 – Q1)/sqrt(n), extreme of the upper whisker: Q3 + 1.58 * (Q3 – Q1)/sqrt(n), n = 5. e, Mutation burden and copy number analysis of gastric lesions (n=5).

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