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来自化石燃料的芳烃与乳腺癌

Aromatics from fossil fuels and breast cancer.

作者信息

Hilakivi-Clarke Leena, Jolejole Theresa Krista, da Silva Joas Lucas, de Oliveira Andrade Fabia, Dennison Gail, Mueller Steffen

机构信息

The Hormel Institute, University of Minnesota, 801 16 Avenue NE, Austin, MN 55912, USA.

Department of Food Science and Nutrition, University of Minnesota, 1334 Eckles Avenue, St Paul, MN 55108, USA.

出版信息

iScience. 2025 Mar 10;28(4):112204. doi: 10.1016/j.isci.2025.112204. eCollection 2025 Apr 18.

Abstract

Polycyclic aromatic hydrocarbons (PAHs) from fossil fuels initiate breast cancer in animal models, and in humans a link between PAH exposure and breast cancer risk has been established. In women, it takes approximately two decades for PAH-exposed breast cells to progress to diagnosable breast cancer, and the exposure needs to happen during a time window when breast is vulnerable to PAHs. Further, not everyone exposed to high levels of PAHs develops breast cancer. PAHs are most likely to lead to breast cancer initiation among individuals who were exposed through pregnant mothers to environmental pollutants or maternal obesity or both. These early life exposures are shown to increase daughter's later susceptibility to breast cancer by causing in the daughter (1) an increase in the number of structures in the breast in which breast cancer initiation takes place, (2) a suppression, perhaps epigenetically, in the ability of cells to repair DNA damage caused by PAHs by inhibiting expression of tumor suppressor genes, or (3) a persistent gut dysbiosis, which then impacts immune cells in the tumor microenvironment. Among the early life environmental pollutants that increase breast cancer susceptibility may be volatile aromatic BTEX compounds. Thus, aromatics from fossil fuels are likely to be involved in causing breast cancer, and efforts should be directed toward reducing human exposure to these compounds to prevent breast cancer.

摘要

化石燃料中的多环芳烃(PAHs)可在动物模型中引发乳腺癌,并且在人类中已证实PAH暴露与乳腺癌风险之间存在联系。在女性中,接触PAH的乳腺细胞大约需要二十年时间才能发展为可诊断的乳腺癌,而且这种暴露需要在乳腺对PAHs敏感的时间窗口内发生。此外,并非所有接触高剂量PAHs的人都会患乳腺癌。PAHs最有可能在那些通过母亲在孕期接触环境污染物或母亲肥胖或两者兼而有之的个体中引发乳腺癌。这些早期生活暴露通过以下方式增加女儿日后患乳腺癌的易感性:(1)使女儿乳腺中发生乳腺癌起始的结构数量增加;(2)可能通过表观遗传方式抑制细胞修复PAHs所致DNA损伤的能力,这是通过抑制肿瘤抑制基因的表达实现的;或者(3)导致持续的肠道菌群失调,进而影响肿瘤微环境中的免疫细胞。增加乳腺癌易感性的早期生活环境污染物中可能包括挥发性芳香族BTEX化合物。因此,化石燃料中的芳烃很可能与乳腺癌的发生有关,应致力于减少人类对这些化合物的接触以预防乳腺癌。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e105/11985079/dd535ec6d712/fx1.jpg

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