Dietary mutagen exposure and risk of pancreatic cancer
Dietary mutagen exposure and risk of pancreatic cancer
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DOI：
10.1158/1055-9965.epi-06-0993
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发表时间：
2007-04-01
影响因子：
3.8
通讯作者：
Hassan, Manal M.
中科院分区：
文献类型：
--
作者：
Li, Donghui;Day, Rena Sue;Hassan, Manal M.
为了调查饮食中食物诱变剂暴露与胰腺癌风险之间的关系，我们于2002年6月至2006年5月在德克萨斯大学安德森癌症中心进行了一项以医院为基础的病例对照研究。共有626例病例和530名非癌症对照组在种族、性别和年龄(+/-5岁)方面进行了频率匹配。膳食暴露信息是通过使用肉类准备问卷的个人访谈收集的。与对照组相比，显著更多的病例显示出更喜欢熟猪肉、培根、烤鸡和平底锅炸鸡，而不是汉堡和牛排。与对照组相比，患者每天的食物诱变剂摄入量和诱变活性(每克肉类摄入量中的回复因子)都更高。调整其他混杂因素后，2-amino-3，4，8-trimethylimidazo[4，5-f]quinoxaline(DiMeIQx)和苯并(A)芘(BaP)的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)。五分位数分析显示，随着DiMeIQx摄入量的增加，癌症风险显著增加(P-趋势=0.024)。在没有癌症家族史的人中，饮食中较高的诱变剂摄入量(前两个五分之一)与胰腺癌风险增加2倍相关，但在有癌症家族史的人中则不相关。在暴露于PhIP和BaP最高水平(前10%)的个体中，观察到饮食诱变剂暴露和吸烟可能存在协同效应。P-交互作用分别为0.09和0.099。这些数据支持这样一种假设，即饮食中单独接触诱变剂以及与其他因素相互作用有助于胰腺癌的发展。
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.