1990 Fiscal Year Final Research Report Summary
Identification of a Chromosome Carrying a Putative Tumor Suppressor gene in Human Choriocarcinoma by Microcell-Mediated Chromosome Transfer.
| Project/Area Number |
63480363
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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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 (1989-1990)
Hokkaido University (1988) |
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Principal Investigator |
WAKE Norio Medical Institute of Bioregulation Kyushu Univ., 生体防御医学研究所, 教授 (50158606)
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| Co-Investigator(Kenkyū-buntansha) |
IMAMURA Toshiro Medical Institute of Bioregulation Kyushu Univ., 生体防御医学研究所, 助手 (10221095)
MIYAMOTO Shingo Medical Institute of Bioregulation Kyushu Univ., 生体防御医学研究所, 助手 (40209945)
KATO Hidenori Medical Institute of Bioregulation Kyushu Univ., 生体防御医学研究所, 助手 (60214392)
IWANAGA Tomohisa Medical Institute of Bioregulation Kyushu Univ., 生体防御医学研究所, 助手 (80213304)
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| Project Period (FY) |
1988 – 1990
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| Keywords | Hydatidiform mole / Choriocarcinoma / Cell fusion / Microcell fusion / Tumor / Suppressing gene / cDNA expression libraries specific to #7 / Gene cloning |
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| Research Abstract |
There are two main mechanisms of origin for complete hydatidiform mole ; a) fertilization of an empty egg by a haploid sperm followed by duplication and b) fertilization of such an egg by two haploid spermatozoa. It is widely accepted that of all forms of pregnancy that had to choriocarcinoma the risk associated with moles is by far the highest. Homozygous expression of a recessive mutation of moles has been assumed to associate with this propensity to malignancies.
Alterations of several tumor suppressor genes together with activation of oncogenes are assumed to be necessary for choriocarcinogenesis. Genetic characteristics shown in the moles suggest that the former alterations are especially important to explore the multistep conversions to malignancies. Thus, individual chromosomes derived from normal cells were introduced into choriocarcinoma cells via microcell fusion. Evaluation of tumorigenicity in microcell hybrids suggested that chromosome #7 carried a putative tumor suppressor gene for choriocarcinoma. The gene imprinting or recessive mutation mmy be responsible for the inactivation of such a gene. Being able to correspond with the high propensity to malignancy of moles. Now, the cDNA expression liberaties specific to the normal #7 chromosome could be produced. Colony hybridization using mRNA probes obtained from normal villi and CCI choriarcinoma in addition to suicide selection cloning the revertant will be able to clone the tumor suppressor genes of choriocarcinoma.
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