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. 2018 Nov 1;32(21-22):1420–1429. doi: 10.1101/gad.314286.118

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© 2018 Aubrey 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. — Mutant TRP53 proteins do not accelerate lymphoma development in the Trp53^−/− and Trp53^+/− genetic backgrounds. (A) HSPC reconstitution model to examine the impact of mutant TRP53 protein expression on tumor development. (B) The mutant TRP53 proteins studied, with the corresponding human amino acid position indicated. (*) Hot spot mutation. (C–F) Kaplan-Meier survival curves for mice reconstituted with Trp53^−/− (C,D) or Trp53^+/− (E,F) HSPCs transduced with empty vector (pMIG) or expression vectors for each of the five mutant TRP53 proteins that were tested. (n) Number of mice. C and E represent composite survival curves of all TRP53 mutants (N = 5) combined. P-values were determined by log rank (Mantel-Cox) test. (G) Tumor phenotype summary for mutant TRP53 transduced Trp53^+/− HSPC reconstitution experiments (from E and F). The tumor spectra for the individual TRP53 mutants are shown in Supplemental Figure S1G.