| Project/Area Number |
20790990
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Thoracic surgery
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| Research Institution | Yamaguchi University |
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Principal Investigator |
TANAKA Tosiki Yamaguchi University, 大学院・医学系研究科, 助教 (50457305)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 癌 / DNA損傷 / Biomarker / DNA損傷応答 |
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| Research Abstract |
Lung adenocarcinoma tissue samples were obtained from the surgical resected specimen. The tissues were classified into 3 groups according to pathology : normal lung parenchyma, bronchiolo-alveolar carcinoma and adenocarcinoma. We evaluated DNA damage response (DDR) proteins, phosphorylated ataxia telangiectasia mutated (pATM), phosphorylated H2AX (γH2AX) and Chk2 (pChk2) protein levels by immunohistochemistry. Immunostaining for pATM and pChk2 revealed that they tended to be expressed during tumor progression in advanced carcinoma although there were no significant differences. However, γH2AX was little expressed and there was no correlation with tumor progression. There was no correlation between DDR and clinical factors.
ATM and Chk2 was activated during cancer progression, but little H2AX was detected. It is likely that activation of DDR was induced by stress signaling as a consequence of oxidative, replication and mechanical stresses occurring during growth and expansion of the lung adenocarcinoma. DDR may be related to cancer progression.
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