| Project/Area Number |
06671638
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Gifu University School of Medicine |
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Principal Investigator |
FUJIMOTO Jiro Gifu University, School of Medicine, Assistant Professor, 医学部附属病院, 講師 (80199372)
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| Co-Investigator(Kenkyū-buntansha) |
TAMAYA Teruhiko Gifu University, School of Medicine, Professor, 医学部, 教授 (70079870)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Uterine Endometrial Cancer / Uterine Leiomyoma / Ovaian Cancer / Sex Steroid Receptors / Oncogenes / Tyrosine kinase C / protein Kinase / Molecular Biology / 子宮内膜癌 / 子宮頚癌 / 卵単癌 / 浸潤・転移 / 抗ステロイド / エストロゲン受容体 / プロゲステロン受容体 / アンドロゲン受容体 |
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| Research Abstract |
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.
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