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. Author manuscript; available in PMC: 2013 Sep 16.
Published in final edited form as: Oncogene. 2006 Feb 23;25(8):1272–1276. doi: 10.1038/sj.onc.1209144

Figure 3.

Figure 3

Resistance to DMBA-induced tumorigenesis and increased apoptosis in epidermal keratinocytes for K5-Cre;C/EBPβfl/fl mice. (a) DMBA/TPA skin tumorigenesis study. Wild type, K5-Cre, C/EBPβfl/fl, and K5-Cre;C/EBPβfl/fl mice (6-8 weeks old, six to eight mice per group) were initiated with a single dose of 200 nmol DMBA/200 μl acetone, followed 1 week late with thrice weekly treatment with 5 nmol 12-O-tetradecanoylphorbol-13-acetate (TPA)/200 μl acetone. All experiments were conducted in compliance with institutional guidelines. (b) Apoptosis in DMBA treated skin. Mice (three mice/group) were treated with 200 nmol DMBA/200 μl acetone or with acetone alone. Dorsal skins were collected 24 h after treatment and fixed in 10% neutral buffered formalin. The number of apoptotic keratinocytes/cm length of epidermis was determined as described (Zhu et al., 2002). Interfollicular keratinocytes were scored from three H&E stained sections (~1.5 cm length)/mouse using the following criteria; presence of dark pyknotic nuclei, cytoplasmic eosinophilia and the absence of cellular contacts. Data are expressed as mean±s.d. of three mice. * significantly different from all other DMBA-treated groups (P<0.01) as determined by Student’s t test.