| Project/Area Number |
03670778
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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 | Nagoya University |
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Principal Investigator |
GOTO Setsuko Nagoya University, Caooleg of medical Technology, Professor, 医療技術短期大学部, 教授 (80111847)
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| Co-Investigator(Kenkyū-buntansha) |
KATO Noriko Nagoya University, School of Medicine, Medical Staff(Senior Resident), 医学部, 医員
YAMAMURO Osamu Nagoya University, School of Medicine, Assistant, 医学部, 助手 (10240079)
MANO Hisao Nagoya University, School of Medicine, Associate Professor, 医学部, 講師 (00209678)
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| Project Period (FY) |
1991 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1993: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1992: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1991: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Choriocarcinoma / DNA polymorphism / VNTR / MHC / EGF / Autocrine mechanism / Metastasis / Collagenase activity / Interferon / Zymography / 絨毛癌細胞 / コラゲナーゼ活性 / DNA 多型性 / EGFR / 免疫療法 |
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| Research Abstract |
(1) In three cases of choriocarcinoma, genetic loci including a variable number of tandem repeat regions were amplified by the polymerase chain reaction method on DNA from three established cell lines and from lymphocytes of patients and their husbands to identify the responsible pregeacy. In case 1, tumor cells was found to be parental origin and derived from the pregnancy with full-term fetal death. In case 2 and 3, tumor cells were probable androgenetic origin respectively, and were derived from the pregnancy with compiete hydatidiform mole. We also conducted the restriction fragment length polymorphism method using one case samples, and it confirmed the results based on the polymerase chain reaction method producted patterns. All nine cases of hydatidiform mole and three cased of invasive mole were of androgenetic origin.
(2) In examination for the presence of Epidermal Growth Factor (EGF)/Epidermal GRowth Factor REceptor (EGFR) using EGF and 1251-EGF binding assay in conditioned medium. Specific EGF binding sites were observed in these five cell lines. Particularlily, in one cell line, NaUCC-4, we assessed the significance of EGF/EGFR autocrine mechanism.
Immunocytochemical studies of NaUCC-4 cells showed that EGF and EGFR proteins were detected. The addition of monoclonal antibodies (mAbs) against EGF or EGFR inhibited 3H-thymidine incorporation and hCG production dose dependently. These results suggested that EGF might function as an autocrine growth factor in this choriocarcinoma cell line. (3) Choriocarcinoma cells showed high 72kDa geratinase activity, which suggested a role for the enzyme in vascular metasrasis. Studies on use of r IFN-B to inhibit metastasis of choriocarcinoma via supression of geratinase production are warranted.
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