Detection of the molecular target in intractable non-small cell lung cancer
| Project/Area Number |
22590316
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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 |
Human pathology
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| Research Institution | Kyushu University |
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Principal Investigator |
KOGA Takaomi 九州大学, 大学病院, 講師 (70380615)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAGAWA Kazunori 九州大学, 医学研究院, 講師 (50217668)
ONIMARU Mizuho 九州大学, 医学研究院, 助教 (00380626)
OKANO Shinji 九州大学病院, 臨床助教 (10380429)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 呼吸器・縦隔 / 非小細胞肺癌 / 分子標的 / CHFR / ＣＨＦＲ / 異常メチル化 / 肺扁平上皮癌 / メチル化 / EGFR変異 / EML4-ALK / 腺癌 / 喫煙 / 扁平上皮癌 |
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| Research Abstract |
The QG56 cell, which was established from a lung squamous cell carcinoma, with CHFR inactivation due to aberrant methylation was transfected the CHFR expression vector (QG56+). QG56+cells showed suppressed tumor growth rate and cellular motility with statistical significances, and decreased a ratio of multinucleated cells or cells with bizarre nuclei compared with control cells (QG56－) (QG56－24.4%, QG56+3.6%, p<0.05). In flow cytometric analysis, a ratio of aneuploid cells tended to decrease (QG56－10.1%, QG56+1.8%, p=0.08). Our study suggested that retrieval of CHFR expression in NSCLC cells with CHFR loss suppresses tumor aggressiveness. Based on this result, CHFR abnormality might be a therapeutic target.
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Report
(4 results)
Research Products
(21 results)
