Study of mechanisms of development and growth in hormone (especially estrogen) dependent uterine tumor and its related diseases.

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Estrogen iduced testosterone binding sites (TBS) in uterine leiomyoma and endometrium, but not in myometrium. Testosterone downregulated the estrogen-induced TBS.Therefore, responsiveness of leiomyoma to sex steroids might be recognized as an endometrial type (J.Steroid Biochem. Molec.Biol.).Estrogen receptor (ER) mRNA was overexpressed in uterine endometrial cancer than normal endometrium, and it had some point mutations in DNA binding domain (Horm.Res.). Mutations of epidermal growth factor receptor and erbB-2 mRNAs were detected in endometrial cancer, which with mutated ER might contribute to a part of development and growth of this tumor (Eur.J.Gynecol.Oncol.). Estrogen induced expression of c-Ha-ras and c-fos/c-jun mRNAs in uterine endometrial normal and cancer cells via tyrosine kinase and protein kinase C,respectively. Progesterone diminished the estrogen-induced their expressions in normal cells, but not in cancer cells (J.Steroid Biochem.Molec.Biol., Ann.Clin.Biochem.). Therefore, progesterone could not regulate the estrogen-induced oncogene expressons.Expression of progesterone receptor form M mRNA might be related to malignant phenotype of gynecologic cancers, especially ovarian cancers (tumor Biol.). some DNA polymorphism of estrogen and progesterone receptor genes may contribute to invasion and metastasis of gynecologic cancers.