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胰腺癌中吸烟和大量饮酒的流行病学和潜在机制。

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

机构信息

Unit of Nutrition, Environment and Cancer, Epidemiology Research Program, Catalan Institute of Oncology, Bellvitge Biomedical Research Institute, L'Hospitalet de Llobregat, Barcelona, Spain.

出版信息

Mol Carcinog. 2012 Jan;51(1):40-52. doi: 10.1002/mc.20786.

DOI:10.1002/mc.20786
PMID:22162230
Abstract

Tobacco smoking represents an important known cause of ductal pancreatic adenocarcinoma. Recent data from pooled analyses in consortia involving multiple case-control 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.

摘要

吸烟是一种已知的导致导管腺癌的重要原因。最近,多个合作的病例对照和队列研究的汇总分析数据表明,大量(而非适度或少量)饮酒也可能增加胰腺癌的风险。动物和人体证据表明,烟草致癌物和代谢物可能协同作用,并在胰腺癌发生的早期和晚期阶段具有遗传和表观遗传效应。一种更重要的与烟草有关的致癌物 NNK,可能通过多种途径发挥作用。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)的作用来增加胰腺癌的风险,但也可能具有独立的遗传和表观遗传效应。关于烟草和酒精相关胰腺癌发生的动物和人体研究表明,存在多种重叠的机制途径。吸烟和大量饮酒是可预防的暴露因素,如果避免这些因素,将大大降低全球范围内的胰腺癌负担。

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