| Project/Area Number |
60570763
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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 | Hokkaido University |
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Principal Investigator |
WAKE Norio Hokkaido University Medical Hospital,Lecturer, 医学部附属病院, 講師 (50158606)
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| Co-Investigator(Kenkyū-buntansha) |
ICHINOE Kihyoe Hokkaido University,Professor Emeritus, 名誉教授 (90073783)
SAKAI Keiichiro Hokkaido University Medical Hospital,Instructor, 医学部附属病院, 助手 (30186986)
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| Project Period (FY) |
1985 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1987: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1986: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1985: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | choriocarcinoma / oncogene / ゲノム不安定 / choriocarcinoma / oncogene / transformation / Southern blot hybridization / Northern blot hybridization Cell fusion |
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| Research Abstract |
The Present research project was undertaken to explore the mechanism of choriocarcinogenesis. Identification of the oncogene responsible for choriocarcinogenesis was important for this purpose. DNA transfection was performed by the use of NIH3T3 and 4CY-4-3 cell. The latter was incompletely transformed cell induced by adenovirus type4. However, DNA obtained from the foci following the secondary transfection lost the Alu repeat. Thus, Southern and Northern blots were tried in 5 kinds of choriocarcinoma cells in order to investigate rearrangements and expression status of the already-known orcogenes. 11-13 kinds of oncogenes were expressed in various degrees in these cells although rearrangement of c-myc oncogene was observed in one cell. Since expression of such various oncogenes has not been referred in the part, genomic instability in trophoblast was assumed to play an important role for the malignant transformation. A high induction of SCE with the presence of mitomycin C and chromosome aberrations with its absence observed in cells from monospermic, androgenetic mole would support this assumption.
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