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. 2021 Apr 1;35(7-8):512–527. doi: 10.1101/gad.348220.120

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© 2021 Seavey et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 1. — The mouse Wwtr1-Camta1 model produces EHE tumors. (A) Schematic of the mouse model locus and CreER^T2 crosses. (UnRCB) Unrecombined allele, (RCB) recombined allele, (exons 1–2) Wwtr1 exons 1–2, (exon 3) Wwtr1 exon 3, (3′Camta1) Camta1 exon 9-stop codon in exon 24 adjoined to a hGH terminator sequence). (B) Kaplan–Meier curve for the development of EHE subdivided based on the number of WC alleles and CreER^T2 driver. No tumors developed after tamoxifen treatment in mice with only one WC fusion gene allele and one wild-type Wwtr1 allele. (n) Total number of mice of that genotype. (C) Representative gross pathology images of mouse EHE tumors (right) with corresponding normal tissue for comparison (left). (Top) Peritoneal surface/diaphragmatic lesions (CWC). (Bottom) Liver lesions (RWC).