Insufficiency of a novel anti-oncogene and mouse ovarian tumorigenesis

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K15714
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Obstetrics and gynecology
• Research Institution: Miyagi Prefectural Hospital Organization Miyagi Cancer Center
• Principal Investigator: YAMADA Hidekazu 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん薬物療法研究部, 特任研究員 (10254012)
• Co-Investigator(Kenkyū-buntansha): 島 礼 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん薬物療法研究部, 部長 (10196462) ; 伊藤 しげみ 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん薬物療法研究部, 特任研究員 (80600006)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: 卵巣がん / プロテインホスファターゼ

Outline of Final Research Achievements

In order to address the function of protein phosphatase 6 (PP6) loss on K-ras-initiated tumorigenesis in ovary. To do so, we developed tamoxifen-inducible K-rasG12D-expressing mice and double mutant (K-rasG12D-expressing and Ppp6c-deficient) mice in which K-rasG12D expression is driven by the cytokeratin 14 (K14) promoter. Using 8week old and 12 weeks old female mice, intrabursal injection of an adenovirus-Cre construct was conducted. Eight month after the induction, mice were dissected and ovary was examined. Both K-rasG12D-expressing mice and doubly-mutant mice showed no tumors in the ovary. The results showed that K-rasG12D expression using this system is not sufficient to develop ovarian tumors in mice.

Free Research Field

医歯薬学