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

Figure 1.

Figure 1

Pot1a and p53 cooperate in endometrial carcinogenesis. X-gal-stained uterine sections from 12-week-old mice. (a) Rosa26 LacZ reporter (R26R). (b) Sprr2f-Cre; R26R, showing Cre activity in both surface and deep endometrial glands. Scale bar=100 μℳ for (a) and (b). (c) PCR for floxed (left) and null (right) Pot1a alleles from Sprr2f-Cre; Pot1aL/L; p53L/L mouse tail and uterine tumor. As expected, both control (tail) and tumor samples harbor floxed alleles, since tumor stroma does not undergo gene deletion. However, only tumor DNA harbors the null allele, consistent with endometrial-specific Cre activity. (d) Tumor incidence in aging cohorts at 3, 9 and 15 months. (e) Kaplan–Meier survival analysis for aging cohorts of Sprr2f-Cre; Pot1aL/L vs. Sprr2f-Cre; Pot1aL/L; p53L/L (P<0.0001 by log-rank test). (f) Uterine weights at 3, 9 and 15 months. (g) Gross uterine pictures representative of n=5 animals analyzed per time point. Weight of uterus shown is indicated in the left lower corner.