Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan.
Division of Cancer Stem Cell, Miyagi Cancer Center Research Institute, 47-1 Nodayama, Medeshima-Shiode, Natori 981-1293, Miyagi, Japan.
Int J Mol Sci. 2024 Jul 18;25(14):7854. doi: 10.3390/ijms25147854.
Chronic infection of is considered the principal cause of gastric cancers, but evidence has accumulated regarding the impact of tobacco smoking and alcohol consumption on the development of gastric cancers. Several possible mechanisms, including the activation of nicotinic acetylcholine receptors, have been proposed for smoking-induced gastric carcinogenesis. On the other hand, local acetaldehyde exposure and ethanol-induced mucosal inflammation have been proposed as the mechanisms involved in the development of gastric cancers in heavy alcohol drinkers. In addition, genetic polymorphisms are also considered to play a pivotal role in smoking-related and alcohol-related gastric carcinogenesis. In this review, we will discuss the molecular mechanisms involved in the development of gastric cancers in relation to tobacco smoking and alcohol consumption.
被认为是胃癌的主要病因,但有越来越多的证据表明吸烟和饮酒也会导致胃癌。有几种可能的机制被提出用于解释吸烟引起的胃癌发生,包括烟碱型乙酰胆碱受体的激活。另一方面,局部乙醛暴露和乙醇引起的黏膜炎症被认为是导致重度饮酒者发生胃癌的机制。此外,遗传多态性也被认为在与吸烟和饮酒相关的胃癌发生中起关键作用。在这篇综述中,我们将讨论与吸烟和饮酒相关的胃癌发生的分子机制。