环境致癌物诱发肺癌的肿瘤遗传学研究

Victor D. Martinez, Adam P Sage, E. Marshall, Miwa Suzuki, A. A. Goodarzi, G. Dellaire, W. Lam
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引用次数: 2

摘要

非烟草诱导的原发性肺肿瘤的分子格局显示出特定的癌遗传学特征。这些肿瘤的病因在很大程度上与暴露于氡、砷和石棉等公认的环境肺癌物质有关。环境致癌物可诱导肺组织发生特异性遗传和表观遗传改变,导致肺癌致癌基因和抑癌基因功能异常。这些分子事件导致关键细胞机制的破坏,如抗氧化应激和DNA损伤修复,从而促进肿瘤的发生和进展。本章提供了与暴露于氡、砷和石棉有关的具体致癌机制的全面讨论。本文还总结了受这些环境因子影响的主要蛋白质编码基因和非编码基因,以及促进其在肺癌中失调的潜在分子机制。最后,本章探讨了非烟草诱导肺癌个性化干预策略的预期挑战。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oncogenetics of Lung Cancer Induced by Environmental Carcinogens
The molecular landscape of non-tobacco-induced primary lung tumors displays specific oncogenetic features. The etiology of these tumors has been largely associated with exposure to well-established environmental lung carcinogens such as radon, arsenic, and asbestos. Environmental carcinogens can induce specific genetic and epigenetic alterations in lung tissue, leading to aberrant function of lung cancer oncogenes and tumor suppressor genes. These molecular events result in the disruption of key cellular mechanisms, such as protection against oxidative stress and DNA damage-repair, which promotes tumor development and progression. This chapter provides a comprehensive discussion of the specific carcinogenic mechanisms associated with exposure to radon, arsenic, and asbestos. It also summarizes the main protein-coding and non-coding genes affected by exposure to these environmental agents, and the underlying molecular mechanisms promoting their deregulation in lung cancer. Finally, the chapter examines the anticipated challenges in personalized intervention strategies in non-tobacco-induced lung cancer.
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