前立腺がんにおけるTMPRSS2およびETS転写因子遺伝子の再発性融合
Scott A Tomlins1, Daniel R Rhodes, Sven Perner
1Department of Pathology, University of Michigan Medical School, 1301 Catherine Street, Ann Arbor, MI 48109-0602, USA.
Science (New York, N.Y.)
|October 29, 2005
まとめ
研究者らは,前立腺がんにおける特定の遺伝子融合 (TMPRSS2-ERG/ETV1) を発見し,これはアンドロゲン反応性要素によって引き起こされる. これらの再編成は一般的であり,がんの発達に影響を与え,新しい診断および治療目標を提供します.
科学分野:
- 遺伝学 遺伝学とは
- 腫瘍学 腫瘍学
- バイオインフォマティックス
背景:
- 繰り返される染色体再編成は,一般的な癌ではよく理解されていません.
- 腫瘍性異常を特定することは,がんの発症を理解するために極めて重要です.
研究 の 目的:
- バイオインフォマティクスアプローチを用いて前立腺がんにおける腫瘍性染色体異常候補を特定する.
- ETS転写因子を含む再発性遺伝子融合を特徴付けるために.
主な方法:
- 異常遺伝子発現のバイオインフォマティクス分析.
- 遺伝子再配列を検出するための光 in situ ハイブリダイゼーション (FISH).
- プロモーター活動の調査のための細胞系実験.
主要な成果:
- ERGとETV1は,前立腺がんにおける異常なETS転写因子として特定されました.
- TMPRSS2 (5' UTR) のERGまたはETV1への再発性遺伝子融合が発見されました.
- ERGまたはETV1の再編成は,前立腺がんの29のサンプルのうち23に存在しました.
- アンドロゲン反応性TMPRSS2プロモーター要素は,ETS過剰発現を媒介する.
結論:
- TMPRSS2-ERG/ETV1遺伝子の融合は前立腺がんではよく見られる.
- これらの再編成は,アンドロゲン反応性プロモーターによって引き起こされます.
- この発見は,がんの発症,分子診断,前立腺がんの治療に影響を及ぼします.
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