Fig. 3
Hormone receptor status changes during GEM mammary tumor progression depending on genotype and is maintained in orthotopic tumors. A Loss of hormone receptor expression in B1/P model occurs after progression from MIN to carcinoma stage. Comparison of the hormone receptor expression in normal gland, in early and in late-stage lesions in B1/P/Rbf and B1/P models is shown. Scale bar 200 µm. B Summary of allograft lines derived from GEM tumors and comparison of their latencies to GEM models. Latencies for allografts are averages from N = 5 mice. C–D Growth of ER + allograft tumors was not inhibited by tamoxifen treatment, or by implanting tumor cells into pre-ovariectomized mice. C B1/P/Rbf cells (passage 1) from the 210,904 tumor line were implanted intraductally into strain-matched recipient mice and treated with tamoxifen, or were implanted into ovariectomized recipients. Differences in survival were not significant by the Log-rank (Mantel-Cox) test, D P/Rbf cells (passage 2, freshly dissociated cells) from the 290,860 tumor line were implanted intraductally into strain-matched recipient mice and treated with tamoxifen, or were implanted into ovariectomized recipients. Ovariectomized mice survived longer than controls (the difference was significant by the Log-rank (Mantel-Cox) test), but all tumors grew to endpoint