Inhibition of tumor angiogenesis activity by medroxyprogesterone acetate in gynecologic malignant tumors.

More than 30% of the colony formation of dispersed tumor cells was inhibited by medroxyprogesterone acetate (MPA) in 2 out of 6 cases of endometrial cancer, in 1 out of 6 cases of cervical cancer, and in 3 out of 12 cases of ovarian cancer. The colony formation inhibited by MPA was not related to clinical stage or histological type. There was no significant difference in the tumor angiogenesis factor (TAF) activity of any case of endometrial, cervical and ovarian cancer between the cortisol-treated group and the controls. TAF activity was inhibited by MPA in 4 out of 6 cases of endometrial cancer, in 5 out of 6 cases of cervical cancer, and in 9 out of 12 cases of ovarian cancer. There was no significant difference in the fibroblast growth factor (FGF) activity of any case of endometrial, cervical and ovarian cancer between the cortisol-treated group and the controls. FGF activity was inhibited by MPA in 3 out of 6 cases of endometrial cancer, in 5 out of 6 cases of cervical cancer, and in 10 out of 12 cases of ovarian cancer. The cases in which the colony formation was inhibited by MPA were not related to the cases in which TAF or FGF activity was inhibited by MPA. Therefore, MPA may reduce neovascularization induced by TAF and FGF, and can depress secondary spreading of some endometrial, cervical and ovarian cancer via the mechanism of terminal process of secondary spreading, regardless of the presence of glucocorticoid actions similar to that of cortisol, and the reduction of cell proliferation.