| Project/Area Number |
12670504
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Sapporo Medical University School of medicine |
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Principal Investigator |
WATANABE Naoki Sapporo Medical University School of Medicine, Department of Laboratory Diagnosis, Professor, 医学部, 教授 (10158644)
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| Co-Investigator(Kenkyū-buntansha) |
KOBAYASHI Daisuke Sapporo Medical University School of Medicine, Department of Laboratory Diagnosis, Instructor, 医学部, 助手 (50295359)
YAGIHASHI Atsuhito Sapporo Medical University School of Medicine, Department of Laboratory Diagnosis, Assistant Professor, 医学部, 講師 (40260757)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2000: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | pancreatic cancer / telomerase / telomeric-repeat binding factor / telomere length / hTERT / TRF1 / TRF2 / TIN2 / 膵癌 |
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| Research Abstract |
To understand the mechanism for maintenance of telomeres, we performed measurement for gene expression for telomerase components, and telomeric-repeat binding factor and its associated protein. Telomerase activity has been found in almost cancers but not in adjacent normal cells. However, telomerase activity did not correlate with telomere length in cancer cells. The results suggest that telomere length may not be regulated by telomerase alone. TRF1, TRF2, and TIN2 are negative regulators of telomere length, and tankyrase and Rapl act as positive regulators. TRF1, TRF2, and TIN2 RNAs were significantly down-regulated in cancers compared to noncancerous tissues. Neither tankyrase nor Rap1 was up-regulated in cancers.
In addition to reactivation of telomerase, down-regulation of TRF1, TRF2, and TIN2 gene expression may be important to escape from the cell death caused by shortening telomere length in cancers. At present time, therefore hTERT, TRFs and TIN2 may be suitable targets for gene therapy for pancreatic cancer.
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