エピジェネティック・プラスティシティは,細胞間の相互作用により,臓腫瘍形成を誘導する
Cassandra Burdziak1,2, Direna Alonso-Curbelo3,4, Thomas Walle1,5,6,7
1Computational and Systems Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
まとめ
初期の臓がんにおける表遺伝的可塑性は,細胞が様々な状態を採用し,腫瘍の進行に影響を与えます. 細胞の可塑性や 組織の交信を理解することで 新しい検知戦略が生まれます
科学分野:
- 癌 生物学
- エピジェネティクス
- 免疫学
背景:
- 腫瘍を誘発する侮辱に対する細胞の反応は異質であり,早期の腫瘍に特異性のない表皮遺伝的役割が示唆される.
- エピジェネティックな可塑性は,最初は類似した細胞から様々な腫瘍の運命を誘導する可能性があります.
研究 の 目的:
- 初期の臓がんにおける表遺伝的可塑性の起源と影響を調査する.
- 細胞状態と組織レベルでの相互作用が 臓新生病を誘発することを特定する.
主な方法:
- 正常,炎症,前悪性,悪性臓組織の単細胞分析
- クロマチンの再構成分析 細胞間のコミュニケーションの場所
- シグナル伝達遺伝子のモジュールと組織のクロストークを特定するための推論アプローチ.
主要な成果:
- 特定された異質な細胞状態は,異なる腫瘍の運命のために準備されています.
- 細胞状態の異質性は,通信場所でのクロマチンの改造と関連している.
- ネオプラジアを誘発する 副皮質細胞と免疫細胞のフィードバックループが マウスで確認されました
結論:
- 臓がんの 組織改造プログラムを発見した
- エピジェネティックな可塑性と細胞間のコミュニケーションは,早期の腫瘍の進行において極めて重要です.
- このプログラムでは 臓がんを検知する 標的となる可能性があります
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