| Project/Area Number |
18591547
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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 |
Thoracic surgery
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| Research Institution | Kobe University |
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Principal Investigator |
MANIWA Yoshimasa Kobe University, Graduate School of Medicine, Assistant Professor (50362778)
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| Co-Investigator(Kenkyū-buntansha) |
OKITA Yutaka Kobe University, Graduate School of Medicine, Professor (40322193)
HAYASHI Yoshitake Kobe University, School of Medicine, Professor (50189669)
吉村 雅裕 神戸大学, 大学院医学系研究科, 講師 (70324910)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,070,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥570,000)
Fiscal Year 2007: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2006: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | lung cancer / risk factor / DNA damage repair gene / single nucleotide polymorphism |
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| Research Abstract |
In this study, we identified gene alterations in lung cancer patients, not from the perspective of acquired mutations caused by various external insults or damaging agents, but from the perspective of hereditary predisposition. We evaluated all the non-synonymous SNPs in the DNA damage repair genes that are present in the available databases, which should allow us to detect those that are closely related with the development of lung adenocarcinoma. Finally, we will organize the data statistically and systematically to facilitate the prediction of a patient's cancer risk. As a results, we confirmed that nonsynonymous SNPs (XRCCI: Arg194Trp, TDG: Gly199Ser, RAD9: His239Arg, POLδ1: Arg119His) were present significantly more frequently in lung cancer patients than in a control group. Alignment analysis revealed that all of the region that contained the SNPs conserved among vertebrates, and the allele frequency is less than 1 % in a normal control population. These findings suggest that this SNP may cause an alteration in the biological activity of the expressed protein. These SNPs may allow to predict the susceptibility of lung cancer in a healthy person.
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