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ID 49253
JaLCDOI
フルテキストURL
Thumnail 67_1_19.pdf 5.17 MB
著者
Furukawa, Masashi Department of Thoracic Surgery, Okayama University Hospital
Soh, Junichi Department of Thoracic Surgery, Okayama University Hospital
Yamamoto, Hiromasa Department of Thoracic Surgery, Okayama University Hospital
Ichimura, Kouichi Department of Pathology, Okayama University Hospital
Shien, Kazuhiko Department of Thoracic Surgery, Okayama University Hospital
Maki, Yuho Department of Thoracic Surgery, Okayama University Hospital
Muraoka, Takayuki Department of Thoracic Surgery, Okayama University Hospital
Tanaka, Norimitsu Department of Thoracic Surgery, Okayama University Hospital
Ueno, Tsuyoshi Department of Thoracic Surgery, Okayama University Hospital
Asano, Hiroaki Department of Thoracic Surgery, Okayama University Hospital
Tsukuda, Kazunori Department of Thoracic Surgery, Okayama University Hospital
Toyooka, Shinichi Department of Thoracic Surgery, Okayama University Hospital
Miyoshi, Shinichiro Department of Thoracic Surgery, Okayama University Hospital
抄録
Nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α (NFKBIA), which is a tumor suppressor gene, was found to be silenced in lung adenocarcinomas. We examined NFKBIA expression, mutations in the EGFR and K-ras genes, and EML4-ALK fusion in 101 resected lung adenocarcinoma samples from never-smokers. NFKBIA expression was evaluated using immunohistochemistry. NFKBIA expression was negative in 16 of the 101 samples (15.8%). EGFR and K-ras mutations and EML4-ALK fusion were detected in 61 (60.5%), 1 (1.0%), and 2 (2.0%) of the 101 samples, respectively, in a completely mutually exclusive manner. Negative NFKBIA expression was observed significantly more frequently among the tumors with none of the three genetic alterations compared to those with such alterations (p=0.009). In addition, negative NFKBIA expression was significantly more frequent among the EGFR-wild type samples compared to the EGFR-mutant samples (p=0.013). In conclusion, NFKBIA expression was silenced in adenocarcinomas without EGFR/K-ras mutations or EML4-ALK fusion, suggesting that the silencing of NFKBIA may play an important role in the carcinogenesis of adenocarcinomas independent of EGFR/K-ras mutations or EML4-ALK fusion.
キーワード
never-smoker
lung cancer
adenocarcinoma
nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α
epidermal growth factor receptor
Amo Type
Original Article
発行日
2013-02
出版物タイトル
Acta Medica Okayama
67巻
1号
出版者
Okayama University Medical School
開始ページ
19
終了ページ
24
ISSN
0386-300X
NCID
AA00508441
資料タイプ
学術雑誌論文
言語
English
著作権者
CopyrightⒸ 2013 by Okayama University Medical School
論文のバージョン
publisher
査読
有り
PubMed ID
Web of Sience KeyUT
関連URL
http://ousar.lib.okayama-u.ac.jp/metadata/52534