Epidemiology and potential mechanisms of tobacco smoking and heavy alcohol consumption in pancreatic cancer

Epidemiology and potential mechanisms of tobacco smoking and heavy alcohol consumption in pancreatic cancer
复制标题

DOI:
10.1002/mc.20786
复制
发表时间:
2012-01-01
影响因子:
4.6
通讯作者:
Duell, Eric J.
Duell, Eric J.
中科院分区:
医学2区
文献类型:
--
作者:
Duell, Eric J.

文献摘要

被引文献

相似文献

吸烟是已知的导致胰腺导管腺癌的重要原因。来自多个病例对照和队列研究的联合汇总分析的最新数据表明,大量(但不是中度或轻度)饮酒也可能增加胰腺癌的风险。动物和人类证据表明,烟草致癌物和代谢物可能在胰腺肿瘤发生的早期和晚期协同作用,并具有遗传和表观遗传效应。与烟草有关的更重要的致癌物之一NNK可能通过多种途径起作用。大量饮酒可能通过增强其他风险因素(如吸烟、营养不良和与慢性胰腺炎相关的炎症途径)的影响而增加胰腺癌风险,但也可能具有独立的遗传和表观遗传影响。动物和人类对烟草和酒精相关的胰腺癌发生的研究表明,多模式,重叠的机制途径。吸烟和大量饮酒是可预防的接触,避免这些接触将大大减少全世界胰腺癌的负担。(C) 2011 Wiley期刊公司
Tobacco smoking represents an important known cause of ductal pancreatic adenocarcinoma. Recent data from pooled analyses in consortia involving multiple casecontrol and cohort studies suggest that heavy (but not moderate or light) alcohol consumption also may increase pancreatic cancer risk. Animal and human evidence indicate that tobacco carcinogens and metabolites may act in concert and have both genetic and epigenetic effects at early and later stages in pancreatic tumorigenesis. One of the more important tobacco-related carcinogens, NNK, probably acts via multiple pathways. Heavy alcohol consumption may increase pancreatic cancer risk by potentiating the effects of other risk factors such as tobacco smoking, poor nutrition, and inflammatory pathways related to chronic pancreatitis, but also may have independent genetic and epigenetic effects. Animal and human studies of tobacco- and alcohol-related pancreatic carcinogenesis suggest multi-modal, overlapping mechanistic pathways. Tobacco smoking and heavy alcohol consumption are preventable exposures, and their avoidance would substantially decrease the burden of pancreatic cancer worldwide. (C) 2011 Wiley Periodicals, Inc.