Li Donghui, Day Rena Sue, Bondy Melissa L, Sinha Rashmi, Nguyen Nga T, Evans Douglas B, Abbruzzese James L, Hassan Manal M
Department of Gastrointestinal Medical Oncology, Unit 426, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):655-61. doi: 10.1158/1055-9965.EPI-06-0993.
To investigate the association between dietary exposure to food mutagens and risk of pancreatic cancer, we conducted a hospital-based case-control study at the University of Texas M. D. Anderson Cancer Center during June 2002 to May 2006. A total of 626 cases and 530 noncancer controls were frequency matched for race, sex and age (+/-5 years). Dietary exposure information was collected via personal interview using a meat preparation questionnaire. A significantly greater portion of the cases than controls showed a preference to well-done pork, bacon, grilled chicken, and pan-fried chicken, but not to hamburger and steak. Cases had a higher daily intake of food mutagens and mutagenicity activity (revertants per gram of daily meat intake) than controls did. The daily intakes of 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx) and benzo(a)pyrene (BaP), as well as the mutagenic activity, were significant predictors for pancreatic cancer (P = 0.008, 0.031, and 0.029, respectively) with adjustment of other confounders. A significant trend of elevated cancer risk with increasing DiMeIQx intake was observed in quintile analysis (P(trend) = 0.024). A higher intake of dietary mutagens (those in the two top quintiles) was associated with a 2-fold increased risk of pancreatic cancer among those without a family history of cancer but not among those with a family history of cancer. A possible synergistic effect of dietary mutagen exposure and smoking was observed among individuals with the highest level of exposure (top 10%) to PhIP and BaP, P(interaction) = 0.09 and 0.099, respectively. These data support the hypothesis that dietary mutagen exposure alone and in interaction with other factors contribute to the development of pancreatic cancer.
为了研究饮食中接触食物诱变剂与胰腺癌风险之间的关联,我们于2002年6月至2006年5月在德克萨斯大学MD安德森癌症中心开展了一项基于医院的病例对照研究。总共626例病例和530例非癌症对照按照种族、性别和年龄(±5岁)进行频数匹配。通过使用肉类制备问卷的个人访谈收集饮食接触信息。与对照组相比,病例组中明显有更大比例的人偏好熟透的猪肉、培根、烤鸡和煎鸡,但不包括汉堡和牛排。病例组的食物诱变剂每日摄入量和诱变活性(每克每日肉类摄入量的回复突变体数)高于对照组。在调整其他混杂因素后,2-氨基-3,4,8-三甲基咪唑[4,5-f]喹喔啉(DiMeIQx)和苯并(a)芘(BaP)的每日摄入量以及诱变活性是胰腺癌的显著预测因素(P分别为0.008、0.031和0.029)。在五分位数分析中观察到随着DiMeIQx摄入量增加癌症风险升高的显著趋势(P趋势 = 0.024)。在没有癌症家族史的人群中,较高的饮食诱变剂摄入量(最高的两个五分位数)与胰腺癌风险增加2倍相关,但在有癌症家族史的人群中并非如此。在对PhIP和BaP暴露水平最高(前10%)的个体中观察到饮食诱变剂暴露与吸烟之间可能存在协同效应,交互作用P值分别为0.09和0.099。这些数据支持了这样的假设,即单独的饮食诱变剂暴露以及与其他因素的相互作用会导致胰腺癌的发生。