Elucidation of the molecular mechanism of endometriosis focusing on epithelial cells.

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K11218
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Obstetrics and gynecology
• Research Institution: The University of Tokyo
• Principal Investigator: HIRATA TETSUYA 東京大学, 医学部附属病院, 登録研究員 (30431860)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: 子宮内膜症 / 月経困難症 / GWAS / PAX8 / IFITM1 / ALDH1A

Outline of Final Research Achievements

To elucidate the pathogenesis of endometriosis, it is essential to focus on the epithelial cells of endometriosis. We focused on the properties of endometriotic epithelial cells. In addition, we focused on epithelial cells of extragenital endometriosis, and found that PAX8 is a highly sensitive endometriotic epithelial marker. We also demonstrated that IFITM1 can be used as a novel endometriosis stromal cell marker. In addition, a genome-wide association analysis of dysmenorrhea revealed an association with LOCUS associated with NGF, IL1A, and IL1B. Further studies will be conducted based on these results.

Free Research Field

子宮内膜症

Academic Significance and Societal Importance of the Research Achievements

子宮内膜症に対する新規病理診断マーカーを見出した。これにより、診断が難しい稀少部位子宮内膜症の病理診断がより正確になり、術後にホルモン療法が必要な患者を正確に抽出し、子宮内膜症の増悪や再発の抑制につながると考える。また、月経困難症とNGFやIL1の関連を見出したことで、早期診断法や新規治療法の開発につながると考える。