Runx3-null mice are resistant to DMBA/TPA tumorigenesis but susceptible to 3′-MCA–induced skin tumors. Runx3-null mice are resistant to DMBA/TPA tumorigenesis.

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Runx3-null mice are resistant to DMBA/TPA tumorigenesis but susceptible to 3′-MCA–induced skin tumors. Runx3-null mice are resistant to DMBA/TPA tumorigenesis but susceptible to 3′-MCA–induced skin tumors. A, representative mice showing multiple papillomas on a WT versus a single papilloma on a Runx3-null mouse at 20 weeks after DMBA initiation. B and C, delayed onset, reduced yield (multiplicity), and decreased rate of papillomas in DMBA/TPA–treated Runx3-null (B) and Runx3fl/fl/Pgk-cre mice (n = 7, each), compared with WT (n = 10) and control (n = 9; bearing ≥1 WT allele) littermate mice, respectively. D, similar papilloma yield, rate, and kinetics in DMBA/TPA–treated Runx3fl/fl/K14-cre mice (n = 10) and WT littermate mice (n = 16). E, macro appearance of an autochthonous fibrosarcoma developing in a WT mouse lower back (left, circled). A section through this tumor (right) shows its subcutaneous localization (H&E, ×63) and the proliferating cancerous fibroblasts (inset, H&E ×400; bar, 50 μm); E, epidermis; D, dermis; M, hypodermal muscle; FS, fibrosarcoma. F, tumor formation kinetics and frequency following 3′-MCA injection. Shown are cumulative tumor numbers/injection sites (%) over time. Left, low dose (50 μg; 11 Runx3-null and 14 WT mice). Right, high dose (100 μg; 10 Runx3-null and 11 WT mice). Values in B–D are mean ± SD. Omri Bauer et al. Cancer Prev Res 2014;7:913-926 ©2014 by American Association for Cancer Research