2004 Fiscal Year Final Research Report Summary
Study of gentic and epigenetic alterations in prostatic cancer using DNA microarray method.
| Project/Area Number |
14370513
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Yamaguchi University |
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Principal Investigator |
NAITO Katsusuke Yamaguchi University, School of Medicine, Professor, 医学部, 教授 (60115251)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUYAMA Hideyasu Yamaguchi University, School of medicine, Associate Professor, 医学部, 助教授 (70209667)
YOSHIHIRO Satoru Yamaguchi University, University Hospital, Assistant Professor, 医学部附属病院, 講師 (40284260)
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| Project Period (FY) |
2002 – 2004
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| Keywords | prostate cancer / primary structure of genom / array CGH / ZD1839 / PC-3 / LNCap / DU-145 / signal transduction |
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| Research Abstract |
Incidence of prostate cancer in Japan and resultant mortality rates are lower than in Western countries. To elucidate the reasons behind this, the genetic characteristics of prostate cancer in Japanese patients were investigated. Comparative genomic hybridization was applied in 27 cases of prostate cancers in Japanese patients. The frequency of 13q loss may imply differences in biological behavior of prostate cancer between Japan and Western coutries. To clarify a array comparative genomic hybridization(CGH) technique, we applied array CGH spotted with 283 specific genes to 11 clinical prostate cancers, and the results were compared with comparative genomic hybridization (conventional CGH) and loss of heterozygosity (LOH) analysis using miciosatellite DNA markers. When the results of both CGH techniques were compared with those of LOH analysis, the correspondence rate of array CGH was significantly higher than that of conventional CGH (93.4% vs. 72.2%, p<0.05).
We examined the antiproliferative effects and mechanism of gefitinib (Iressa, ZD1839), an epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) on three human prostate cancer cell lines, LNCap (hormon-dependent growth), PC-3 (hormone-independent growth) and DU-145. A significant dose-dependent growth-inhibitory effect was observed in the gefinitib treatment group for each cell lines. cDNA microarray experiments showed that several genes were down regulated.
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