Hormone-Induced Protection of Mammary Tumorigenesisin Genetically Engineered Mouse Models - Genetic Engineering: Recent Developments in Applications - page 275

Figure 3 and Table 1. In the control transplants, 10/20 (50%) produced tumors
by 48 weeks after transplantation, with an initial tumor latency of 24 weeks. In
the transplants exposed to hormone combination when they were actively filling
the fat pad, the tumor incidence was 3/20 (15%), with an initial tumor latency of
44 weeks. In contrast, the transplants exposed to the hormone combination much
later after transplantation had an initial tumor latency equivalent to the controls,
but the final tumor incidence (4/20; 20%) was not significantly different (p >
0.05) from that in the group exposed to hormones early after transplantation. The
transplants exposed to tamoxifen for only 3 months did not develop any tumors
after 50 weeks. This experiment demonstrates that a short-term treatment admin-
istered at either the actively proliferating or the steady-state stage of mammary
development can delay tumorigenesis.
Figure 3. The effect of duration of hormone exposure on tumorigenesis in p53-null mammary epithelial
transplants. The effect of hormone exposure was compared with that of a hormone receptor antagonist,
tamoxifen. Mice treated with estradiol and progesterone, either early or late, or treated with tamoxifen, had
a significant decrease in tumor incidence (p < 0.05). Filled circles and solid line, control; filled circles and
dotted line, early hormone exposure; inverted triangles and broken line, late hormone exposure; upright triangle,
tamoxifen. The flow diagram illustrates the experimental treatment plan.
effect of Hormone Pretreatment of the Host on tumorigenesis
in P53-null Mammary epithelium
The tumorigenic capability of the p53-null mammary epithelial cells either direct-
ly exposed to estrogen/progesterone or just to the estrogen/progesterone-treated