2005 Fiscal Year Final Research Report Summary
Significance of hRad9 expression in non-small cell lung cancer cells
| Project/Area Number |
16591395
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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, 大学院・医学系研究科, 助手 (50362778)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIMURA Masahiro Kobe University, Graduate School of Medicine, Associate Professor, 大学院・医学系研究科, 講師 (70324910)
OKITA Yutaka Kobe University, Graduate School of Medicine, Professor, 大学院・医学系研究科, 教授 (40322193)
HAYASHI Yoshitake Kobe University, School of Medicine, Associate Professor, 医学部, 教授 (50189669)
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| Project Period (FY) |
2004 – 2005
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| Keywords | DNA damage / lung cancer / hRad9 |
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| Research Abstract |
hRad9 accumulation was observed in the nuclei of tumor cells in 33% of all nonsmall cell lung carcinoma (NSCLC) specimens examined, and elevated levels of phosphorylated hRad9 were found to be associated with the detection of phosphorylated Chk1. To the authors' knowledge, the current study was the first to describe the overexpression of hRad9 in surgically reseated tumor specimens and its phenotypic significance in tumor cells.
Sequence analyses of the HRAD9 gene derived from 50 surgical specimens of lung adenocarcinoma were performed to investigate the status of this gene. Analysis of the coding regions indicated that there was no alteration in the HRAD9 sequence. Quantitative polymerase chain reaction of mRNA revealed that the gene was transcribed in all samples examined. However, these studies detected the presence of a nonsynonymous single nucleotide polymorphism (His239Arg) that occurred with a high frequency. This polymorphism appears to be associated with an increased risk of lung adenocarcinoma.
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Research Products
(4 results)
