| Project/Area Number |
14571568
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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 |
Obstetrics and gynecology
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| Research Institution | Kyushu University |
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Principal Investigator |
SONODA Kenzo Kyushu University, Faculty of Medicine, Assistant Professor, 大学病院, 助手 (30294929)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAMOTO Shingo Kyushu University, Faculty of Medicine, Lecturer, 大学病院, 講師 (40209945)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2002: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | Gynecologic oncology / Invasion / Metastasis / Anoptosis / Tumor stroma / Lymphocyte / Fibroblast / Molecular biology / 腫瘍間質 |
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| Research Abstract |
(1) RCAS1 expression in uterine endometrial cancer : Immunohistochemical analysis, using 147 patients' samples, showed that overexpression of RCAS1 was significantly correlated with age at surgery, stage, extent of myornetrial invasion, and positive peritoneal cytologic results. Multivariate analysis revealed that RCAS1 expression and metastasis were clinically significant prognostic factors for overall survival. These findings indicated that analysis for RCAS1 expression can provide crucial information about the clinical behavior of uterine endometrial cancer, which may be valuable for management of patients with this disease.
(2) RCAS1 induces microenvironmental change in uterine cancer : (1)RCAS1 associated with tumor size. (2)RCAS1 related with the number of lymphocyte apoptosis in metastatic lymph nodes, (3)RCAS1 expression induced reduction of vimentin positive tumor stromal cells, (4)RCAS1 was correlated with tumor VEOF expression and stromal microvessel density. Accumulating these data, RCAS1 might play a pivotal role in tumor invasion and metastasis. (5)Serum RCAS1 level was measured by ELISA analysis. RCAS1 level was significantly higher in uterine cancer patients than in healthy donors. RCAS1 level changed in response to clinical inanifestation increased in recurrence, and decreased after effective treatments. Moreover, serum RCAS1 induced apoptosis of putative receptor-expressing K562 cells in vitro. These data indicated that RCAS1 might be a novel biomarker in management of uterine cancer patients.
(3) Several basic studies are now under investigation : (1)The analysis of phenotype and signal transduction mechanism of RCAS1, by using truncation mutant transfected cells, and (2)Isolation of protease which induces proteolytic processing of RCAS1.
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