通过空气污染物促进肺腺癌
William Hill1, Emilia L Lim1,2, Clare E Weeden1
1Cancer Evolution and Genome Instability Laboratory, The Francis Crick Institute, London, UK.
Nature
|April 5, 2023
概括
空气污染,特别是细颗粒物 (PM2.5),通过激活肺细胞中已经存在的突变来促进肺癌. 这项研究将空气质量与癌症发展联系起来,
科学领域:
- 环境健康
- 癌症学
- 分子生物学
背景情况:
- 环境暴露导致癌症的机制尚不完全理解.
- 瘤生成通常被视为涉及遗传突变和随后的推广的多步骤过程.
- 空气污染,特别是PM2.5是肺癌的已知危险因素.
研究的目的:
- 研究PM2.5在促进肺癌中的作用,特别是EGFR驱动的病例.
- 阐明PM2.5暴露可能启动或促进肺瘤形成的细胞和分子机制.
- 在组织学上正常的肺组织中确定致癌驱动突变的流行率.
主要方法:
- 对大量患者 (32,957例) 的分析,以将PM2.5水平与EGFR驱动的肺癌发病率相关联.
- 使用功能性小鼠模型研究空气污染物对肺组织的生物学影响.
- 通过对295个个体的正常肺组织进行超深突变分析.
主要成果:
- 在较高的PM2.5水平和EGFR驱动的肺癌发病率增加之间发现了显著的关联.
- 在小鼠模型中,PM2.5暴露诱导了巨细胞的流入,IL- 1β的释放,以及EGFR突变肺细胞中的前代细胞状态.
- 在很大一部分健康肺组织样本中检测到先前存在的瘤突变 (EGFR在18%,KRAS在53%).
结论:
- 通过向已存在瘤突变的肺细胞,PM2.5充当瘤促进剂.
- 这些发现突显出空气污染与肺癌发展之间存在关键联系,
- 减少空气污染对于减轻全球肺癌负担至关重要.
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