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. 2011 Jul 15;6(7):e21877. doi: 10.1371/journal.pone.0021877

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This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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A, In vivo phenotype of ΔNp63α-overexpressing keratinocytes in the presence and absence of oncogenic ras. Primary mouse keratinocytes were infected with lentivirus encoding lenti-GFP or lenti-ΔNp63α or sequentially with retrovirus encoding v-ras^Ha followed by lenti-GFP or lenti-ΔNp63α. The final tumor phenotype was assessed at 5 weeks following grafting. Final tumor volumes at 4 weeks are presented as the mean tumor volume ± S.E. B, Upper panel, representative H&E sections of tumor tissues obtained from grafting sites. Lower panel, BrdU incorporation in grafted tissue samples. C, Quantification of BrdU incorporation levels. Data are presented as the mean % of BrdU positive cells ± S.E. * indicates a statistically significant difference between lenti-GFP/v-ras^Ha and lenti-ΔNp63α/v-ras^Ha groups at p<0.05.