development by overcoming resistance to anticancer drugs against ovarian clear cell adenocarcinoma

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592526
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Obstetrics and gynecology
• Research Institution: Kinki University (2014); Nara Medical University (2012-2013)
• Principal Investigator: KANAYAMA Seiji 近畿大学, 医学部附属病院, 講師 (10423914)
• Co-Investigator(Kenkyū-buntansha): SHIGETOMI Hiroshi 奈良県立医科大学, 医学部, 助教 (20433336) ; HARUTA Shouji 奈良県立医科大学, 医学部, 助教 (30448766) ; KOBAYASHI Hiroshi 奈良県立医科大学, 医学部, 教授 (40178330)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 卵巣明細胞腺癌 / 抗がん剤耐性 / HNF1-beta / 細胞周期 / ｃｈｋ１

Outline of Final Research Achievements

As the gene which specifically emerged for an ovarian light cell adenocarcinoma, I identified HNF1-beta. Furthermore, after examining an association between HNF1-beta and DNA damage check mechanism, what the chk1 protein which was a main control factor of the checkpoint mechanism phosphorylated continuously was confirmed with the HNF1-beta-positive cell. Furthermore, participation of the claspin protein became clear in autophosphorylation of chk1. HNF1-beta broke down claspin by some kind of mechanism, and, for the ovarian light cell adenocarcinoma, it restrained it, and it guided the activation that chk1 was superabundant through expression maintenance, and an apoptosis instruction with the action-related bleomycin was inhibited for G2/M period by the examination of conventional us, and it was confirmed to show anticancer agent resistance

Free Research Field

婦人科腫瘍学