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. 2012 Jun 11;32(17):2211–2219. doi: 10.1038/onc.2012.232

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Copyright © 2013 Macmillan Publishers Limited

This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/

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Double-strand DNA breaks in Pot1a p53 tumors. (a–d), γ-H2AX immunohistochemistry, 15-month-old animals. (a) Pot1a^L/L control. (b) Sprr2f-Cre; p53^L/L. (c) Sprr2f-Cre; Pot1a^L/L. (d) Sprr2f-Cre; Pot1a^L/L; p53^L/L. (e–h) Ki67 immunohistochemistry, 15-month-old animals. (e) Pot1a^L/L controls. (f) Sprr2f-Cre; p53^L/L. (g) Sprr2f-Cre; Pot1a^L/L. (h) Sprr2f-Cre; Pot1a^L/L; p53^L/L. (i, j) Percentage of immunopositive nuclei plotted for each genotype at 3, 9 and 15 months (n=5 for each time point). (i) γ-H2AX. (j) Ki67. Size bars=50 μℳ for (a–d) and 100 μℳ for (e–h).