| Project/Area Number |
04404065
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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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 |
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Principal Investigator |
TAMAYA Teruhiko Gifu University School of Medicine, Professor, 医学部, 教授 (70079870)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIMOTO Jiro Gifu University School of Medicine, Assistant Professor, 医学部・附属病院, 講師 (80199372)
IMAI Atsushi Gifu University School of Medicine, Associate Professor, 医学部, 助教授 (40193643)
森 秀弘 岐阜大学, 医学部附属病院, 講師 (50190997)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥13,000,000 (Direct Cost: ¥13,000,000)
Fiscal Year 1994: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1993: ¥5,000,000 (Direct Cost: ¥5,000,000)
Fiscal Year 1992: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | Female Reproductive Organ / Corresponding Benign and Malignant Tumor / Corresponding Circumstance / Tumorigenesis and Proliferation / Sex Steroid Receptors / Oncogenes / Celluar SHBG / CBG / 婦人科腫瘍 / マクロファージ / エストロゲン受容体 / プロゲステロン受容体 / 細胞内CBG / 細胞内SHBG / 子宮内膜 / 子宮内膜癌 / エストロゲン / エストロゲン作用発現機構 / エストラジオール・エストロン |
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| Research Abstract |
In the tissues of female reproductive organs and corresponding benign and malignant tumors and circumstances, cellular profiferation and function are basically regulated by sex steroids, which imply the expressions (mRNA) of cellular oncogenes and steroid receptors, corresponding to mutations.
(1) Synthesis of cellular SHBG/CBG (mRNA) in the uterine endometrium is primarily regulated by estrogen/progesterone. However abandance of SHBG gives the supply of estrogen to the endometriotic tissues.
(2) Monocyte/macrophage in the ascites with pelvic endometriosis is activated, while expression of fms (M-CSF receptor) oncogene is stimulated by estrogen/progesterone, resulting in activation of tyrosine kinase, and anti-estrogenic compound inhites it.
(3) Expressions of Ha-ras, c-myc, fos and jun oncogenes (mRNA) are induced by estrogen in the normal uterus but altered in corresponding benign and malignant tumors due to the difference of estrogen/progesterone effectiveness.
(4) The cellular carcinogenesis and proliferation in endometrial cancer are partly related to estrogen action, which involves the pointmutations in the estrogen receptor domains and delations ofextracellular domains of erbB-1 and erbB-2 products, and overexpression of progesterone B type (proliferation) instead of A type (inhibition).
Accumulation o those abnormalities of gene expressions might be related to the cancer events.
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