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単細胞配列解析によるトリプルネガティブ乳がんにおける化学抵抗性の進化

Charissa Kim¹, Ruli Gao², Emi Sei²

¹Department of Genetics, UT MD Anderson Cancer Center, Houston, TX 77030, USA; Graduate School of Biological Sciences, UT MD Anderson Cancer Center, Houston, TX 77030, USA.

|April 24, 2018

まとめ

トリプルネガティブ乳がん (TNBC) の化学療法耐性は,新しい遺伝的変化ではなく,既存の耐性細胞クローンから生じる. これらの抵抗性遺伝子型は治療によって選択され,細胞は化学療法中に遺伝子発現に適応します.

科学分野:

腫瘍学
ゲノミクス
癌生物学

背景:

トリプルネガティブ乳がん (TNBC) は,頻繁に化学療法に抵抗することが知られている攻撃的なサブタイプです.
この抵抗性の起源 (既にあるクローンと新しい変異) は,まだ解決されていない重要な問題です.

研究の目的:

TNBCにおける化学療法耐性を引き起こすメカニズムを調査する.
抵抗性の原因としてクローン選択と獲得されたゲノム異常を区別する.

主な方法:

ネオアジュヴァント化学療法 (NAC) を受けている20人のTNBC患者の縦断プロファイリング.
大量エクソームシーケンシング,単細胞DNAシーケンシング (900細胞),単細胞RNAシーケンシング (6,862細胞) の適用.

主要な成果:

深層エクソームシーケンシングは10人の患者でクローン絶滅と10人の患者でNAC後のクローン持続を明らかにした.
単細胞分析では,耐性遺伝子型が既に存在し,NACによって適応的に選択されていることが示された.
転写プロフィールは,化学療法への反応として細胞の再プログラムによって得られた.

結論:

TNBCにおける化学療法耐性は,主に既存の耐性クローンの適応的選択によって引き起こされる.
細胞の再プログラムと獲得された転写プロファイルは,TNBCの治療反応と抵抗に寄与する.

キーワード:

乳がんゲノミクス癌アヌプロイド症化学療法コピー数の進化腫瘍内異質性シングルセルシーケンシング治療に対する耐性トリプルネガティブ乳がん腫瘍の進化

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