このエントリーをはてなブックマークに追加
ID 33002
フルテキストURL
著者
Yano, Masaaki Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
Ouchida, Mamoru Department of Molecular Genetics, Graduate School of Medicine and Dentistry, Okayama University 科研費研究者番号
Shigematsu, Hisayuki Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
Tanaka, Noriyoshi Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
Ichimura, Koichi Department of Pathology, Graduate School of Medicine and Dentistry, Okayama University
Kobayashi, Kazuyasu Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
Inaki, Yasuhiko Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
Toyooka, Shinichi Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
Tsukuda, Kazunori Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
Shimizu, Nobuyoshi Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
Shimizu, Kenji Department of Molecular Genetics, Graduate School of Medicine and Dentistry, Okayama University 科研費研究者番号
抄録
In an attempt to identify tumor suppressor genes on chromosome 10 in non-small cell lung cancers, we isolated 10 types of splicing variants of the HELLS/ SMARCA6 gene transcripts. HELLS/SMARCA6 is a novel member of SNF2 family, which is implicated in cellular function like chromatin remodeling. Variant 1 was an alternatively spliced isoform containing an insertion of a 44-ntd intronic sequence between exons 3 and 4, giving rise to a premature termination of translation. The expression of the variant 1 was detected exclusively in the lung cancer specimens (11 of 43 cases, 26%), but was not detected in corresponding normal tissues. D10S520 marker in the proximity of the HELLS/SMARCA6 gene showed prevalent allelic loss (41%) as compared with flanking markers (25-31%). These results suggest that loss of function of HELLS/SMARCA6 by allelic loss and aberrant proteins by tumor-specific exon creation may result in epigenetic deregulation, leading the lung cells to malignancy or its progression.
キーワード
alternative splicing
HELLS
loss of heterozygosity
lung cancer
SMARCA6
備考
Digital Object Identifer:10.1002/ijc.20407
Published with permission from the copyright holder. This is the author's copy, as published in the Journal of International Journal of Cancer, October 2004, Volume 112, Issue 1, Pages 8-13.
Publisher URL:http://dx.doi.org/10.1002/ijc.20407
Direct access to Thomson Web of Science record
Copyright © 2004 Wiley-Liss, Inc. All rights reserved.
発行日
2004-10-20
出版物タイトル
International Journal of Cancer
112巻
1号
出版者
Wiley-Liss, Inc.
開始ページ
8
終了ページ
13
ISSN
0020-7136
NCID
AA00680002
資料タイプ
学術雑誌論文
言語
English
OAI-PMH Set
岡山大学
著作権者
Wiley-Liss, Inc.
論文のバージョン
author
PubMed ID
DOI
Web of Sience KeyUT