1996 Fiscal Year Final Research Report Summary
Establishment of gene diagnosis and therapy for Endometrial carcinoma.
| Project/Area Number |
07457391
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
WAKE Norio Medical Institute of Bioregulation Kyushu Univ. Professor, 生体防御医学研究所, 教授 (50158606)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIDA Jun-ichi Medical Institute of Bioregulation Kyushu Univ. Lecturer, 生体防御医学研究所, 助手 (40264113)
KATO Kiyoko Medical Institute of Bioregulation Kyushu Univ. Lecturer, 生体防御医学研究所, 助手 (10253527)
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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| Project Period (FY) |
1995 – 1996
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| Keywords | Chromosome 1 / Tumor suppressor gene / asingle chromosome transfer / Ras / Estrogen Receptor / Transcription factor / Endometrial Carcinoma |
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| Research Abstract |
1. We made various fragments derived from a human chromosome 1 by high dose radiation, and transferred them into endometrial carcinoma cells via microcell fusion. The introduction of a whole chromosome 1 resulted in the morphological alteration followed by cell senescence. In addition, telomerase activity was also suppressed in the microcell hybrids containing a chromosome 1. Evaluation of cell morphology in addition to telomerase activity in the microcell hybrid clones containing various fragments form chromosome 1 disclosed that 1q11-q21 or q31-ter region of chromosome 1 was critical for the suppression of endometrial cell growth properties.
2. We established the reconstituted cells expressing that mutant K-Ras protein constitutively. Enchanced expression of ER protein that has a function as a transcription factor was shown in this cell. We also established the reconstituted cells expressing both the wild type of K-Ras protein and ER protein. Long term culture in the presence of 10% calf serum transformed the cell that was analogous to the level in the mutant K-Ras expressing cells, was shown in this transformed cells. These implicate ER protein in Ras-mediated transformation.
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