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2018 Fiscal Year Final Research Report

Analysis of tumor suppression mechanism via cell competition of ARID1A in epithelial ovarian cancer

Research Project

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Project/Area Number 15K20166
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Obstetrics and gynecology
Research InstitutionSt. Marianna University School of Medicine

Principal Investigator

Uekawa Atsushi  聖マリアンナ医科大学, 医学部, 研究技術員 (60534253)

Project Period (FY) 2015-04-01 – 2019-03-31
KeywordsARID1A
Outline of Final Research Achievements

In many human cancers, activation of oncogenes and loss of function of tumor suppressor genes cause tumorigenesis of cells. In clear cell ovarian cancer, the tumor suppressor gene ARID1A is frequently mutated to a defective function. Among the cancer suppression functions of ARID1A, this research was conducted based on the new concepts of cell growth control and cell competition. As a result, it was found that cells deficient in the ARID1A gene proliferate more dominantly than non-deficient cells. Furthermore, we identified changes in gene expression that occur in cells deficient in the ARID1A gene.

Free Research Field

婦人科腫瘍学

Academic Significance and Societal Importance of the Research Achievements

卵巣癌の中の一つのタイプである卵巣明細胞癌は、既存の抗癌剤に抵抗性を示す難治性の疾患である。日本における卵巣明細胞癌の発生頻度は、卵巣癌全体の25%を占め、欧米の8%と比べても極めて高く、近年急速に増加している。そのため、卵巣明細胞癌に対する新たな治療法開発のための基礎研究が、特に日本において重要な研究課題である。本研究は、卵巣明細胞癌の発症メカニズムの一端を解析したものであり、このメカニズムの理解は、新たな治療薬、予防薬の開発に繋がる可能性があることから臨床的に貢献できる。

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Published: 2020-03-30  

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