ADAR1 induced somatic hypermutation in ovarian endometriosis

• Project/Area Number: 25861470
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Obstetrics and gynecology
• Research Institution: Chiba University
• Principal Investigator: TSURUOKA Nobuhide 千葉大学, 医学部附属病院, 医員 (50375763)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Project Status: Completed (Fiscal Year 2014)
• Budget Amount: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000); Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000); Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
• Keywords: 体細胞突然変異 / 卵巣がん

Outline of Final Research Achievements

Ovarian cancer does occur at higher than expected rates in women with endometriosis. ARID1A and c-myc have high frequent mutations in ovarian clear cell carcinoma. The RNA editor gene ADAR1 is induced by inflammatory ligands and buffers stress response. The ADAR1 gene was overexpressed in endometriosis and ovarian clear cell carinoma cells.Exogenous ADAR1 induced adenosine-targeted DNA mutations in the ARID1A gene and the c-myc gene of wild-type mouse embryonic fibroblasts (MEFs) which have γ-H2AX expression.