| Project/Area Number |
17591685
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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 |
Urology
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| Research Institution | Nagasaki University |
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Principal Investigator |
SAKAI Hideki Nagasaki University, Graduate School of Biomedical Sciences, Associate Professor (40235122)
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| Co-Investigator(Kenkyū-buntansha) |
KANETAKE Hiroshi Nagasaki University, Graduate School of Biomedical Sciences, Professor (50100839)
IGAWA Tsukasa Nagasaki University, University Hospital of Medicine and Dentistry, Senior Assistant Professor (40295069)
MIYATA Yasuyoshi Nagasaki University, Graduate School of Biomedical Sciences, Assistant Professor (60380888)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2006: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Prostate cancer / Knock-in mouse / cDNA microarray analysis / β・microseminoprotein / PSP94 / Ultrasonography |
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| Research Abstract |
1. To study the biological characteristics of a new knock-in mouse adenocarcinoma of the prostate (KIMAP) model, we performed a comparative study with mice from both the KIMAP and transgenic mouse adenocarcinoma of the prostate (TGMAP) models.
(1) The KIMAP tumors demonstrated a tumor architecture of heterogeneity and multifocality similar to that of human prostate cancer compared with TGMAP model.
(2) Comparative studies on cDNA microarrays demonstrated that KIMAP tumors were upregulated with higher contents of immunoresponse genes, whereas TGMAP tumors had neuroendocrine (NE) differentiation.
(3) Several tumor marker genes characteristic of human prostate cancer were uniquely identified in KIMAP tumors, including hepsin, maspin, Nkx3.l, CD10 and PSP94, etc.
Due to the similarities between human prostate cancers and the KIMAP tumors, this preclinical model may supplement the current transgenic models to study the prostate cancer more accurately.
2. To investigate the use of mouse PSP94 as a serum biomarker for mouse prostate cancer model studies, we quantified PSP94 levels in the mouse serum with competitive ELISA techniques. Compared with wild-type mice, serum PSP94 levels increased significantly with tumor grade, tumor weight and age in KIMAP mice. Through longitudinal monitoring of serum PSP94 levels of castrated mice, we found a correlation between responsiveness/refractory prostate tissues and serumPSP94 levels. The utility of mouse serumPSP94 as a marker in hormone therapy was confirmed.
3. We assessed the usefulness of transrectal ultrasonography (TRUS) imaging with a fine ultrasound probe for measuring prostate cancer progression in the KIMAP model.
(1) A scanning frequency of 30 MHz was found to be best for screening of prostate cancer in mice.
(2) TRUS imaging could identify tumors with a minimum size of 1.0 mm diameter.
(3) TRUS allows a longitudinal observation of prostate cancer progression in mice.
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