| Project/Area Number |
06671663
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
ARIMA Takahiro Medical Institute of Bioregulation Kyushu Univ.Lecturer, 生体防御医学研究所, 助手 (80253532)
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| Co-Investigator(Kenkyū-buntansha) |
WAKE Norio Medical Institute of Bioregulation Kyushu Univ.Professor, 生体防御医学研究所, 教授 (50158606)
KATO Kiyoko Medical Institute of Bioregulation Kyushu Univ.Lecturer, 生体防御医学研究所, 助手 (10253527)
今村 利朗 九州大学, 生体防御医学研究所, 助手 (10221095)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Genomic Imprinting / Human placenta / Androgenetic mole / Choriocarcinoma / Suppressorgene / ゲノムインプリンティング |
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| Research Abstract |
(1) We investigated IGF2 and H19 expression in human placenta, androgenetic mole and choriocarcinoma. Although paternal IGF2 and maternal H19 alleles were exclusively transcribed in full-term placentae, both H19 alleles were active in some specimens of 6-8 weeks gestation. H19 expressed in moles notwithstanding their androgenetic origin, in addition, choriocarcinoma showed biallelic low expression of IGF2 and high expression of H19. The active H19 allele was unmethylated in placentae and moles as expected, but was heavily methylated in choriocarcinomas. These findings may help elucidate the regulatory mechanism of the IGF2-H19 complex and the role of methylation in the control of H19 expression.
(2) The genetic origin of 24 trophoblastic neoplasms was determined using PCR polymorphisms. The main findings of this work were (1) discordance of the antecedent pregnancy with the responsible pregnancy was noted in 3 choriocarcinomas and one PSTT.(2) in 8post molar trophoblastic neoplasia, 6 had developed egg devoid of nuclei fertilized by X-bearing sperm. The remaining 2 showed DNA polymorphisms compatible with mole derived from dispermic fertilization of empty eggs. (3) nongestational 3 choriocarcinomas were assumed to arise from a germ cell after meiosis I.
(3) We will try to find the putative choriocarcinoma suppressor gene on human chromosome7 using STS marker, we found deletion region, D7S633 near centromere of chromosome7 in 7 choriocarcinoma cell lines. 4 YAC clones including D7S633 and ERV3 has been isolated. Now, we investigated the introduction of these clones into cell lines and has been isolated cDNA using Exon trapping technique.
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