| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Outline of Final Research Achievements |
Intratumoral cortisol concentration was considered to be regulated by 11β-hydroxysteroid dehydrogenase (HSD) 1 and 11β-HSD2 in endometrial cancer. In endometrial cancer, cortisol induced enzymatic activity of estrogen synthase (aromatase) through glucocorticoid receptor (GR) located in the stromal cells but nor carcinoma cells. This finding suggests that cortisol contributed estrogen-dependency of endometrial cancer cells. It is also suggested that cortisol directly relates to cell growth through the induction of annexin A1 expression, which is known as a GR target gene, in stromal cells of endometrial cancer. Dhydroepiandrosterone (DHEA), which is also known as a stress-related hormone, was synthesized by steroid sulfatase in endometrial cancer tissue.
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