OBJECTIVE: We sought to create an animal model for the development of endom
etrial cancer in women with androgen excess. We examined the effects of est
radiol and androgen, both alone and as precursors to estrogen biosynthesis
on human endometrial cancers transplanted into a nude mouse model.
STUDY DESIGN: We transplanted an estrogen-responsive, well-differentiated,
established human endometrial carcinoma, EnCa-101, subcutaneously into athy
mic male nude mice. We established, first, that aromatase was expressed in
this cell line, inducible by estrogen. We measured the growth of the tumor
in the various groups weekly with Vernier calipers. We examined the effects
of estradiol and androgens, both aromatizable and nonaromatizable, on tumo
r growth.
RESULTS: Estrogen-supplemented tumors showed the greatest rate of growth an
d were significantly greater than the growth rate in castrate mice. Androge
n-supplemented tumors showed a growth rate similar to that of tumors withou
t significant hormonal exposure (castrate mice). Dihydrotestosterone had no
effect on tumor growth in comparison with an agonadal state.
CONCLUSIONS: Aromatizable and nonaromatizable androgens have little growth-
promoting effect on a well-differentiated endometrial carcinoma. Estradiol
is the most potent growth stimulus in our model.