Study of gene amplification in ovarian carcinoma and Choriocarcinoma
Project/Area Number |
62570749
|
Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Obstetrics and gynecology
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Research Institution | Nagoya University |
Principal Investigator |
ISHIZUKA Takao Nagoya University, School of Medicine, 医学部, 講師 (70135333)
|
Co-Investigator(Kenkyū-buntansha) |
GOTO Setsuko Nagoya University, School of Medicine, 医学部, 講師 (80111847)
|
Project Period (FY) |
1987 – 1988
|
Project Status |
Completed (Fiscal Year 1988)
|
Budget Amount *help |
¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
|
Keywords | Oncogene / Gene Amplification / Ovarian Carcinoma / 絨毛癌 / 繊毛性疾患 / トランスフォーミング遺伝子 |
Research Abstract |
Amplification of oncogene is thought to be one of mechanisms of initiation and progression of some kinds of malignant tumors. To investigate whether or not this mechanism is involved in the carcinogenesis of malignant ovarian tumors and trophoblastic diseases, 19 of malignant ovarian tumors including borderline malignancy and 4 of benign ovarian tumors, and 5 of choriocarcinoma cell lines, 2 of normal villi, 2 of hydatidiform mole, 2 of invasive mole and 1 choriocarcinoma were tested with various kinds of oncogene probes using southern blotting method. No gene amplification or rearrangement of oncogenes was observed in any above described tumors, sugesting that the mechanism of oncogene amolification is not involved in the initiation and progression of malignant ovarian tumors and trophoblastic diseases. In addition, we attempted to find transforming activity of malignant ovarian tumors using NIH3T3 transforming assay. No transforming activity was observed in 12 of malignant tumors. As to expression of oncogenes, 5 of choriocarcinoma cell lines were tested using northern blotting method and showed various kinds of oncogene expression to various degree as reported so far. To our regret, however, we could not obtain enough specimens of trophoblastic disease. Therefore, the relation Between these expression of various oncogenes and the initiation and progression of trophoblastic disease is still unknown. Further study in many clinical specimens of trophoblastic disease will be necessary to elear this relation.
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Report
(3 results)
Research Products
(6 results)