| Project/Area Number |
09470356
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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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)
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| Project Period (FY) |
1997 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥9,000,000 (Direct Cost: ¥9,000,000)
Fiscal Year 2000: ¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1998: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1997: ¥3,200,000 (Direct Cost: ¥3,200,000)
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| Keywords | female reproductive organ / tumors / stimulation and inhibition of growth / sex steroid / receptor / GnRH / エストロゲン受容体 / スプライシング・バリアント / プロゲステロン受容体A型 / プロゲステロン受容体B型 / 受容体発現異常 / GnRH受容体 / Gタンパク / 女性生殖器腫瘍 / 性ステロイドホルモン / GnRH・レセプター |
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| Research Abstract |
The growth of the female reproductive organs and related tumors is diversely regulated by hormones (steroids and polypeptides) through binding their corresponding cellular receptors, which is thereafter associated with the biological events
As the advance in dedifferentiation and malignancy of the tumors, cellular expressions of decreasing SHBG, increasing estrogen receptor (ER) exon 5 delated splicing variant (dominant positively functional), and decreasing progesterone receptor A (transcriptionally inhibitory) appear as trends.
ER β is expressed in 1 out of 100 ER αs in the normal uterine endometrium and in 1 out of 10 ER α in the normal ovary, yet the ER β expression becomes variably low to high in the malignant transformation, in which ER α-related action might be exaggerated. PR-B and ER α, which are associated with steroid-related growth, are over-expressed in the N1H3T3 cells, which form colonies and over-grow in the nude-mouse.
GnRH and its receptor are expressed in the uterine endometrial and the ovarian cancers, yet a GnRH agonist occupies the receptor, coupled with Gi protein, resulting in the induction of dephospholyrase and lysophosphatidic acid dehydrase. A GnRH agonist induces apoptosis in the receptor carring tumors as well. Those might be related to the suppretion of tumor growth by a GnRH agonist.
In the tumor cells, the cellular maturity process of GnRH is disturbed, whichi is related to the following evidence ; the pro-peptides of GnRH occupies the receptor, resulting the inhibition of cellular GnRH function which might be related the tumor growth.
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