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肝がんにおける腫瘍遺伝子の識別と検証は,統合的腫瘍遺伝学的なアプローチを用いて行われます
Lars Zender1, Mona S Spector, Wen Xue
1Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
Cell
|July 4, 2006
まとめ
この研究では,肝臓がんに対する新しいマウスモデルを導入し,cIAP1とYapを協力する腫瘍遺伝子として特定しました. 彼らの共増幅は腫瘍の成長を促し,ヒトの癌遺伝子を発見するための戦略を提供します.
科学分野:
- 腫瘍学 腫瘍学
- 遺伝学 遺伝学とは
- 分子生物学は分子生物学である.
背景:
- 人間の腫瘍の異質性と不安定性は,ゲノム的な方法のみを使用してがんを誘発する変異の識別を複雑にします.
- 精密な動物モデルを開発することは,肝臓がんの発症と進行を理解するために不可欠です.
研究 の 目的:
- 肝臓がんの研究のための扱えるマウスモデルを確立する.
- 肝細胞癌 (HCC) に関する協力性腫瘍遺伝子を特定し,特徴づけること.
主な方法:
- 病変を誘発する原始細胞を用いた肝がんに対するマウスモデルの生成.
- マウスモデルとヒトHCCサンプルからの腫瘍の全ゲノム分析.
- 増幅されたゲノム領域内の候補腫瘍遺伝子を特定するための遺伝子発現分析.
主要な成果:
- マウス染色体9qA1 (ヒト11q22) の再発増幅は,マウスおよびヒトの両方の肝臓腫瘍で確認されました.
- cIAP1 (アポトーシス阻害剤) とYap (転写因子) は,このアンプリカン内の候補腫瘍遺伝子として特定されました.
- cIAP1とYapの増幅と共同発現は腫瘍形成を加速し,腫瘍の成長に不可欠であり,彼らの協力的な腫瘍学的機能を実証しました.
結論:
- 開発されたマウスモデルは,肝臓がんの研究に貴重なツールを提供します.
- cIAP1とYapは,共増強されたときに腫瘍遺伝子として協力し,肝臓腫瘍発生を誘発する.
- この研究は,共増幅された腫瘍遺伝子の研究を通じて,ヒトの癌遺伝子を特定し,注釈するための効率的な戦略を示唆しています.
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