Wark Petra A, Van der Kuil Wieke, Ploemacher Janneke, Van Muijen Goos N P, Mulder Chris J J, Weijenberg Matty P, Kok Frans J, Kampman Ellen
Division of Human Nutrition, Wageningen University, Wageningen, The Netherlands.
Int J Cancer. 2006 Jul 15;119(2):398-405. doi: 10.1002/ijc.21839.
K-ras mutation-positive (K-ras+) and -negative (K-ras-) colorectal adenomas may differ clinically and pathologically. As environmental compounds may cause mutations in the growth-related K-ras oncogene or affect clonal selection depending on mutational status, we evaluated whether the aetiology of K-ras+ and K-ras- adenomas differs. K-ras mutations in codons 12 and 13 were assessed in colorectal adenoma tissue (K-ras+: n = 81, K-ras-: n = 453). Dietary and lifestyle data were collected through questionnaires that were also administered to 709 polyp-free controls. Multiple logistic regression analyses showed that intake of vitamin B2 and monounsaturated fat were differently associated with risk of K-ras+ and K-ras- adenomas; vitamin B2 was inversely associated with K-ras- (highest vs. lowest tertile: odds ratio (OR) = 0.70, 95% confidence interval (CI) = 0.50-0.97, p trend = 0.020), but not with K-ras+ adenomas, and a positive association with monounsaturated fat was confined to K-ras- adenomas (OR = 1.57, 95% CI = 1.06-2.34, p trend = 0.029). Besides, potential, not statistically significant, differences in risk arose because red meat was distinctly positively associated with K-ras+ adenomas (OR = 1.70, 95% CI = 0.94-3.09, p trend = 0.061); total dietary and polyunsaturated fat tended to be inversely associated with risk of K-ras+ but not of K-ras- adenomas; inverse associations with dairy products, calcium, protein and tea were confined to K-ras- adenomas, and smoking was more markedly positively associated with K-ras- adenomas. No differences in risk of K-ras+ and K-ras- adenomas could be detected for other factors. In conclusion, dietary and lifestyle factors may influence risk of K-ras+ and K-ras- adenomas differently. However, epidemiological literature on diet, lifestyle and colorectal K-ras mutations is inconsistent.
K-ras 突变阳性（K-ras+）和阴性（K-ras-）的大肠腺瘤在临床和病理方面可能存在差异。由于环境化合物可能导致生长相关的 K-ras 癌基因发生突变，或根据突变状态影响克隆选择，我们评估了 K-ras+和 K-ras-腺瘤的病因是否不同。对大肠腺瘤组织（K-ras+：n = 81，K-ras-：n = 453）中的第 12 和 13 密码子的 K-ras 突变进行了评估。通过问卷调查收集饮食和生活方式数据，该问卷也发放给了 709 名无息肉的对照者。多项逻辑回归分析表明，维生素 B2 和单不饱和脂肪的摄入量与 K-ras+和 K-ras-腺瘤风险的关联不同；维生素 B2 与 K-ras-腺瘤风险呈负相关（最高三分位数与最低三分位数相比：优势比（OR）= 0.70，95%置信区间（CI）= 0.50 - 0.97，p 趋势 = 0.020），但与 K-ras+腺瘤无关，单不饱和脂肪与 K-ras-腺瘤呈正相关（OR = 1.57，95%CI = 1.06 - 2.34，p 趋势 = 0.029）。此外，红肉与 K-ras+腺瘤明显呈正相关（OR = 1.70，95%CI = 0.94 - 3.09，p 趋势 = 0.061），这导致风险出现潜在的、但无统计学意义的差异；总膳食脂肪和多不饱和脂肪与 K-ras+腺瘤风险呈负相关趋势，但与 K-ras-腺瘤无关；与乳制品、钙、蛋白质和茶的负相关仅限于 K-ras-腺瘤，吸烟与 K-ras-腺瘤的正相关更为明显。其他因素在 K-ras+和 K-ras-腺瘤风险方面未检测到差异。总之，饮食和生活方式因素可能对 K-ras+和 K-ras-腺瘤风险产生不同影响。然而，关于饮食、生活方式与大肠 K-ras 突变的流行病学文献并不一致。
