Fig. 1 ∣. Overexpression of Sox2 and loss of Trp53/Cdkn2a give rise to ESCC.

a, Genomic aberrations of TP53, CDKN2A and SOX2 in ESCC samples from TCGA. Each column denotes a tumor. The types of alterations are shown in the marked colors. b, Schematic diagram of generating organoids with different genotypes from mouse esophageal epithelial cells that were isolated from Rosa26^{CAG-loxp-stop-loxp-Sox2-IRES-Egfp} (LSL-Sox2); H11^{CAG-loxp-stop-loxp-Cas9} (LSL-Cos9) mice. CRISPR-mediated knockout of Trp53 and Cdkn2a (p16) or LacZ was introduced to organoids before implantation into nude mice. c, Representative images of hematoxylin and eosin (H&E) and immunohistochemistry (IHC) staining of p63 and Sox2 in engineered organoids. (This experiment was repeated once with similar results.) d, Immunoblots of Sox2, p53 and Cdkn2a in noted engineered organoids. (This experiment was repeated twice with similar results). e, Representative images of orthotopic and subcutaneous tumors from implanted engineered organoids (top) and tumor characteristics (bottom). Each group consists of ten mice, each bearing two tumors. (This experiment was repeated twice with similar results.) f, Representative H&E staining, and Sox2 and Trp63 IHC staining in tumors derived from CPP and SCPP organoids. (This experiment was repeated once with similar results.) N/A, not applicable.