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外分泌機能の変化は,早期の臓がんで脂肪の消耗を誘発する

Laura V Danai¹, Ana Babic², Michael H Rosenthal²

¹Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.

|June 22, 2018

まとめ

臓管内腺がん (PDAC) は,臓機能の低下によって引き起こされる早期の脂肪組織の消耗を引き起こします. 皮肉なことにこの組織喪失を逆転させるとネズミの生存は悪化しますが患者のデータによると生存には影響はありません

科学分野:

腫瘍学
メタボリックシンドローム
癌生物学

背景:

悪性腫瘍は宿主の代謝を変化させ,管腺がん (PDAC) と関連した衰弱症候群を引き起こします.
PDACによって引き起こされる外周組織の衰弱は,患者の生活の質と生存の可能性に悪影響を及ぼします.
組織消耗のための循環要因を標的とした現在の戦略は,限られた臨床的成功を示している.

研究の目的:

早期PDACにおける脂肪組織と筋肉組織の消耗を引き起こすメカニズムを調査する.
PDACに関連した消耗における臓機能と腫瘍の位置の役割を決定する.
PDACモデルと患者の生存に対する組織損失の逆転の影響を評価する.

主な方法:

PDACのマウスモデルを用いて組織の消耗を研究した.
腫瘍の位置 (臓と非臓) が脂肪組織に与える影響を研究した.
臓酵素置換が消耗に与える影響を評価した.
診断時の組織枯渇と生存との相関に関する患者のデータを分析した.

主要な成果:

PDAC腫瘍の成長は特に臓で他の場所ではなく脂肪組織の消耗を誘発します
脂肪組織喪失の主要な要因として,外分泌性臓機能の低下が確認された.
臓酵素置換療法は,PDACに関連した周辺組織損失を軽減しました.
PDACマウスモデルでの脂肪組織損失の逆転が生存率を低下させた.
PDAC患者では,診断時に脂肪および骨格筋組織の枯渇が一般的であったが,生存率の低下とは関連していなかった.

結論:

PDACにおける早期の脂肪組織の消耗は,外分泌臓機能の低下によって説明される.
マウスモデルでの組織喪失の逆転は生存に害を及ぼしますが,患者の生存には影響しない可能性があります.
これらの発見は,PDACカシェキアとその予後的な影響についての洞察を提供します.

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