ID | 49253 |
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フルテキストURL | |
著者 |
Furukawa, Masashi
Department of Thoracic Surgery, Okayama University Hospital
Yamamoto, Hiromasa
Department of Thoracic Surgery, Okayama University Hospital
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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
Kaken ID
Tsukuda, Kazunori
Department of Thoracic Surgery, Okayama University Hospital
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Toyooka, Shinichi
Department of Thoracic Surgery, Okayama University Hospital
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Miyoshi, Shinichiro
Department of Thoracic Surgery, Okayama University Hospital
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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.
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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
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Amo Type | Original Article
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出版物タイトル |
Acta Medica Okayama
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発行日 | 2013-02
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巻 | 67巻
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号 | 1号
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出版者 | Okayama University Medical School
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開始ページ | 19
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終了ページ | 24
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ISSN | 0386-300X
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NCID | AA00508441
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資料タイプ |
学術雑誌論文
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言語 |
英語
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著作権者 | CopyrightⒸ 2013 by Okayama University Medical School
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論文のバージョン | publisher
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査読 |
有り
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PubMed ID | |
Web of Science KeyUT | |
関連URL | http://ousar.lib.okayama-u.ac.jp/metadata/52534
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