| Project/Area Number |
23591149
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kochi University |
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Principal Investigator |
KAMIOKA Mikio 高知大学, 教育研究部医療学系, 助教 (00274374)
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| Co-Investigator(Kenkyū-buntansha) |
DAIBATA Masanori 高知大学, 教育研究部医療学系, 教授 (50263976)
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| Co-Investigator(Renkei-kenkyūsha) |
MURAKAMI Masanao 高知大学, 教育研究部医療学系, 助教 (80571017)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 呼吸器腫瘍 / ウイルス / 感染症 / 癌 / 微生物 / 呼吸腫瘍 |
|---|
| Research Abstract |
Lung cancer is a leading cause of cancer-related mortality. Although smoking is the major risk factor for the development of lung cancer, the number of lung cancers occurring in never smokers has increased in recent times. Factors other than smoking such as oncogenic virus may be associated with the development of lung cancer.
In this study, we tested non-small cell lung cancer (NSCLC) for the presence of Merkel cell polyomavirus (MCPyV) and detected the viral genome in some patients with NSCLC. We showed the presence of integrated MCPyV genome into host cells and a truncated large T gene with a preserved retinoblastoma tumor-suppressor protein-binding domain. Although the viral detection rate was low, the molecular signatures of MCPyV infection support the possibility that during the multistep carcinomagenesis process MCPyV may partly participate in the pathogenesis of NSCLC in a subset of patients.
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