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In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells
Published on: July 23, 2010
型16によるグルココルチコイド依存性腫瘍学的変異であるが,型11ではないヒトパピローマウイルスDNADNAによる変異である
M M Pater1, G A Hughes, D E Hyslop
1Faculty of Medicine, Memorial University of Newfoundland, St. John's, Canada.
Nature
|October 27, 1988
まとめ
ヒトパピローマウイルス (HPV) タイプ16のDNAは,Ha-rasオンコゲンとデキサメタゾンと組み合わせて,原細胞を腫瘍学的に変容させることができます. これは,HPVに関連する子宮頸がんの発症におけるホルモンの役割を示唆しています.
科学分野:
- 腫瘍学 腫瘍学
- ウイルス学 ウイルス学 ウイルス学
- 分子生物学は分子生物学である.
背景:
- 子宮頸部状細胞癌は,女性の一般的な癌であり,ヒトパピローマウイルス (HPV) 感染症と強く相関しています.
- 16型と18型HPVの統合DNAは,子宮頸部腫瘍の大多数で発見されています.
- ホルモンとたばこは,子宮頸症の共因因子であると疑われ,HPV-16ではグルココルチコイド反応要素が特定されています.
研究 の 目的:
- 活性化されたHa-rasオンコゲンと組み合わせたHPV-16DNAの腫瘍性変異の可能性を調査する.
- この変換過程におけるグルココルチコイドホルモンデキサメタゾンの役割を決定する.
主な方法:
- プライマリ細胞はHPV-16DNAと活性化されたヒトHa-ras腫瘍遺伝子を移植した.
- デキサメタゾンが発がん性変異に及ぼす効果を評価した.
主要な成果:
- 主細胞がHPV-16DNA,活性化されたHa-ras,およびデキサメタゾーンに同時に曝露されたとき,腫瘍性変異が観察されました.
- HPV-11のDNAは,同じ条件下で変換を誘導せず,HPV型特異性を示した.
- デキサメタゾンは,観察された腫瘍性変異に不可欠でした.
結論:
- HPV-16 DNA,活性化されたHa-ras,およびデキサメタゾンの組み合わせは,原始細胞の腫瘍性変異を誘発することができます.
- グルココルチコイドホルモンは,HPVに関連した子宮頸がんの発症における重要なコファクターとして作用する可能性があります.
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