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结合流行病学研究结果探讨铬和镍致癌作用中的遗传与细胞机制。

Genetic and cellular mechanisms in chromium and nickel carcinogenesis considering epidemiologic findings.

作者信息

Chiu Arthur, Katz A J, Beaubier Jefferson, Chiu Nancy, Shi Xianglin

机构信息

National Center for Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, Washington, DC 20460, USA.

出版信息

Mol Cell Biochem. 2004 Jan;255(1-2):181-94. doi: 10.1023/b:mcbi.0000007274.25052.82.

Abstract

Genetic and environmental interactions determine cancer risks but some cancer incidence is primarily a result of inherited genetic deficits alone. Most cancers have an occupational, viral, nutritional, behavioral or iatrogenic etiology. Cancer can sometimes be controlled through broad public health interventions including industrial hygiene and engineering controls. Chromium and nickel are two human carcinogens associated with industrial exposures where public health measures apparently work. Carcinogenic mechanisms of these metals are examined by electron-spin-resonance-spectroscopy and somatic-mutation-and-recombination in Drosophila melanogaster in this report. Both metals primarily affect initiation processes in cancer development suggesting important theoretical approaches to prevention and followup.

摘要

遗传和环境相互作用决定癌症风险,但某些癌症的发生主要仅仅是遗传基因缺陷的结果。大多数癌症具有职业、病毒、营养、行为或医源性病因。癌症有时可以通过广泛的公共卫生干预措施来控制,包括工业卫生和工程控制。铬和镍是两种与工业接触相关的人类致癌物,公共卫生措施在这方面显然是有效的。本报告通过电子自旋共振光谱以及黑腹果蝇中的体细胞突变和重组来研究这些金属的致癌机制。这两种金属主要影响癌症发展的起始过程,提示了预防和后续研究的重要理论方法。

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