| Project/Area Number |
13671775
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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 |
Otorhinolaryngology
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| Research Institution | Kanazawa university |
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Principal Investigator |
YOSHIZAKI Tomokazu Kanazawa University Hospital Assistant Professor, 医学部附属病院, 講師 (70262582)
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| Project Period (FY) |
2001 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Epstein-Barr virus / EBERs / MDCK / transformation / PKR / nasopbaryngeal carcinoma / Epstein-Barr virus / EBウイルス |
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| Research Abstract |
EBERs is composed of EBER1 and EBER2. Transfection of EBER1+EBER2 expression vector in MDCK cell enhanced colony formation in soft agar, indicating that expression of EBERs transformed MDCK cell to potentially malignant, anchor-independent phenotype. Either EBER1 or EBER2 expression alone was not sufficient for transformation of MDCK cell to this anchor-independent character. EBERs did not protect MDCK cells from dell death in the condition of serum starvation and irradiation. EBERs are known to activates protein kinase R(PKR) which is activated by double-strand RNA. However, our in vitro kination assay revealed that EBERs did not activate PKR in MDCK cells. These results suggest that transformation of MDCK by EBERs were mediated by alternative pathway rather than PKR pathway. Expression of EBERs in nasopharyngeal carcinoma tissue tended to be correlated with advanced T stage, suggesting that EBERs promote growth and proliferation of tumor cell in nasopharyngeal carcinoma.
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