Akopyan Gohar, Bonavida Benjamin
Department of Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine at UCLA, Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA 90095-1747, USA.
Int J Oncol. 2006 Oct;29(4):745-52.
The deleterious effects of tumor-promoting tobacco carcinogen, nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK, nicotine-derived nitrosamine ketone) have undoubtedly been stipulated. Though many tobacco agents play a part in the development of lung tumors, the potent effects of NNK remain unmatched. It is therefore critical to distinguish the variety of cofactors involved in NNK-mediated pathogenesis, and the unique pathways necessary for successful cellular biotransformation. Current reviews have consistently identified the strengths of NNK and prospective tumor capabilities. Others have delineated specific cellular factors mediating NNK and lung tumors, and have identified metabolic and signaling pathways largely responsible for NNK activation and tumorigenic initiation. Unique to this review is that it summarizes the extensive network of cofactors and cellular mechanisms that promote NNK-specific lung tumorigenesis. As such, it displays a fuller, more comprehensive overview, bringing us one step closer to understanding the fatal consequences of NNK, thus, discovering new avenues that successfully break the cycle of NNK-mediated lung carcinogenesis.
肿瘤促进性烟草致癌物亚硝胺4-(甲基亚硝胺基)-1-(3-吡啶基)-1-丁酮（NNK，尼古丁衍生的亚硝胺酮）的有害影响无疑已得到明确。尽管许多烟草成分在肺肿瘤的发生发展中起作用，但NNK的强大作用仍无可匹敌。因此，区分参与NNK介导的发病机制的各种辅助因子以及成功进行细胞生物转化所需的独特途径至关重要。当前的综述一直确定了NNK的优势和潜在的肿瘤能力。其他人已经描述了介导NNK和肺肿瘤的特定细胞因子，并确定了在很大程度上负责NNK激活和肿瘤发生起始的代谢和信号通路。本综述的独特之处在于，它总结了促进NNK特异性肺肿瘤发生的广泛辅助因子网络和细胞机制。因此，它展示了更全面、更完整的概述，使我们离了解NNK的致命后果又近了一步，从而发现成功打破NNK介导的肺癌发生循环的新途径。
