Tumor escape in a Wnt1-dependent mouse breast cancer model is enabled by p19^Arf/p53 pathway lesions but not p16^Ink4a loss
J. Clin. Invest. Michael T. Debies, et al. 118:51 doi:10.1172/JCI33320 [Go to this article.]

Figure 3
Mammary neoplasia and relapse in Ink4a/Arf-deficient mice. (A) Wnt-initiated mammary hyperplasia. Panels depict carmine-stained whole mounts demonstrating consistent changes in mammary gland morphology in MTB/TWNT mice regardless of Ink4a/Arf gene dosage. (B) Rates of primary mammary tumorigenesis. Cohorts of mice of the indicated genotypes began chronic Dox treatment beginning at 5 weeks of age and were monitored twice weekly for mammary tumors. Bi-Tg, MTB/TWNT bitransgenic; Mono-Tg, monotransgenic. (C) Rates of Dox-independent relapse. Mice harboring biopsy-confirmed mammary tumors were subjected to Dox withdrawal and monitored during periods of tumor regression, remission, and relapse. Relapse-free survival for each cohort was plotted as a function of time, with the day of Dox withdrawal taken as time 0. (D) Tumor growth curves. Tumor volume was plotted as a function of time for representative tumor subsets derived from each cohort.