2006 Fiscal Year Final Research Report Summary
Glucocorticoids induce G1cell cycle arrest in human neoplastic thymic epithelial cells
| Project/Area Number |
17591470
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Thoracic surgery
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| Research Institution | Osaka University |
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Principal Investigator |
SHIONO Hiroyuki Osaka University, Hospital, Specially Appointed Associate Professor (20346216)
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| Co-Investigator(Kenkyū-buntansha) |
OKUMURA Meinoshin Osaka University, Graduate School of Medicine, Associate Professor (40252647)
MINAMI Masato Osaka University, Graduate School of Medicine, Associate Professor (10240847)
INOUE Masayoshi Osaka University, Graduate School of Medicine, Assistant Professor (10379232)
MATSUDA Hikaru Osaka University, Graduate School of Medicine, Professor Emeritus (00028614)
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| Project Period (FY) |
2005 – 2006
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| Keywords | thymoma / thymic epithelial cell / glucocorticoid / glucocorticoid receptor / apoptosis |
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| Research Abstract |
Purpose: Glucocorticoids exert anti-proliferative effects in various cell types and have long been known to induce apoptosis in thymocytes. Although a few reports have described the regression of human thymoma with glucocorticoid therapy, its effects on neoplastic thymic epithelial cells (TECs) have not been reported. In the present study, we investigated glucocorticoid receptor (GR) expression on neoplastic TECs and the effects of glucocorticoids in vitro on the cell cycle progression of tumor cells.
Patients and methods : Thymoma specimens were obtained during surgery from 21 patients. Three of the specimens with glucocorticoid therapy were examined using the TdT-mediated dUTP-biotin nick-end labeling method. Primary tumor specimens from ten untreated thymomas were examined for GR expression by immunohistochemistry. Isolated neoplastic TECs from the remaining eight untreated thymomas were examined using immunohistochemistry, flow cytometric and cell cycle analysis.
Results: GR are expressed on neoplastic TECs as well as on non-neoplastic thymocytes in thymomas, regardless of WHO histological classification. Glucocorticoids caused an accumulation of TEC in GO/G1 phase in all cases examined (n=6), and also induced apoptosis in the three with the lowest levels of Bcl-2 expression.
Conclusions : Our results indicate that neoplastic TECs express GR and that glucocorticoids directly suppress their in vitro proliferation.
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