Project/Area Number |
22591861
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Obstetrics and gynecology
|
Research Institution | Nara Medical University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
KOBAYASHI Hiroshi 奈良県立医科大学, 医学部, 教授 (40178330)
YOSHIZAWA Yoriko 奈良県立医科大学, 医学部, 助教 (80526723)
山田 嘉彦 奈良県立医科大学, 医学部, 講師 (80275346)
|
Project Period (FY) |
2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 卵巣明細胞腺癌 / HNF-1beta / マイクロアレイ / 細胞周期 / 卵巣子宮内膜症性嚢胞 / 癌化 / チェックポイント機構 / 酸化ストレス |
Research Abstract |
Among the ovarian cancers, clear cell adenocarcinoma (CCC) has been recognized as a distinct clinicopathological entity because of its frequent concurrence with endometriotic lesions and its high chemoresistance, resulting in a poor prognosis of high stage tumors. However, the mechanism of resistance in CCC has remained unclear. Hepatocyte nuclear factor-1beta (HNF-1beta) was significantly up-regulated in CCC. Cell cycle arrest induced by DNA damage was maintained by sustained activation of ATM-Chk1 pathway and suppression of cell death in HNF-1beta-overexpressing cells. Chemoresistance of CCC may be the result of aberrant retention of the G2 checkpoint through overexpression of HNF-1 beta. Anticancer agents combined with Chk1 inhibitors may improve the chemosensitivity of CCC.
|