| Project/Area Number |
08671797
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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 | The University of Tokyo |
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Principal Investigator |
TAKAHASHI Satoru The Univ.of Tokyo, Dept.of Urology, Assistant Prof., 医学部・附属病院, 助手 (50197141)
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| Co-Investigator(Kenkyū-buntansha) |
HOMMA Yukio The Univ.of Tokyo, Dept.of Urology, Assistant Prof., 医学部・附属病院, 講師 (40165626)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1996: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | latent prostate cancer / clinical prostate cancer / chromosomes 7,8,10 / microsatellite / allelic imbalance / ヘテロ接合性消失 |
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| Research Abstract |
To evaluate difference of genetic characteristics between clinically insignificant prostate cancer and clinical prostate cancer, we analyzed allelic imbalance (Al) in latent, 'clinically localized, and metastatic prostate cancers. 75 years old or older 32 cases with a latent well-differentiated prostate cancer (tumor volume<0.5ml) found at autopsy were selected as the clinically insignificant cancers for this study. Forty-two clinically localized cancers treated by radical prostatectomy and 20 metastatic prostate cancers were investigated as the clinical cancers. PCR analysis of microsatellite loci mapped to chromosomal regions ; 7q31, 8p22 and 10q23 (PTEN/MMACl gene locus) was performed.
A frequency of AI for at least one marker mapped to 7q31 in latent cancers was 16% of all informative cases, significantly lower than 45% of clinically localized cancers (p<O.Ol) and 65% of metastatic cancers (p<O.OO1). In contrast, frequencies of Al for 8p22-21 in latent and clinically localized cancers were 32% and 43% of all informative cases, respectively (N.S.). Frequencies of AI for 10q23 (PTEN/MMACl gene locus) in latent and clinically localized cancers were low, 9% and 12%, respectively. In contrast, 35% of metastatic cancers cases showed AI, which was significantly higher compared to those of latent and clinically localized cancers.
These results suggest new findings as below.
(1)Chromosomal alterations in clinically insignificant prostate cancers are less frequent than those in clinical cancers.
(2)Inactivation of the putative tumor suppressor gene(s) at 8p22 involves in a large subset of prostate cancer and in early stages of the carcinogenesis.
(3)Genetic alterations at 7q31 and 10q23 (possibly PTEN/MMACI gene mutations) play significant roles in tumor progression and metastasis. Thus, these changes may be useful as genetic markers for clinically significant prostate cancers.
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