Voskuil D W, Kampman E, van Geloof W, Grubben M, Kok F, van Muijen G, Nagengast F, Vasen H, van't Veer P
Division of Human Nutrition and Epidemiology, Wageningen University, The Netherlands.
Dig Dis Sci. 2000 Nov;45(11):2187-94. doi: 10.1023/a:1026485117125.
K-ras and p53 gene mutations are known to occur in high frequencies in sporadic colorectal cancers, but findings are inconsistent in hereditary nonpolyposis colorectal cancer (HNPCC). We compared K-ras codon 12 and 13 gene mutations and p53 protein overexpression in 48 HNPCC (positive for Amsterdam criteria) and 59 sporadic colorectal adenomas, to examine whether they may represent similar or different molecular pathways to cancer. In sporadic adenomas K-ras mutations were detected in 32% and p53 overexpression in 31% of the cases. Similarly, K-ras mutations and p53 overexpression were both found in 25% of HNPCC adenomas. The frequencies of these abnormalities were not significantly different between HNPCC and sporadic adenomas. When taking differences in adenoma size into account, the frequencies were even more similar. In conclusion, these results suggest a similar molecular pathway to adenomas in HNPCC and sporadic carcinogenesis, with respect to involvement of K-ras and p53.
已知K-ras和p53基因突变在散发性结直肠癌中高频发生，但在遗传性非息肉病性结直肠癌（HNPCC）中的研究结果并不一致。我们比较了48例符合阿姆斯特丹标准的HNPCC和59例散发性结直肠腺瘤中K-ras密码子12和13基因突变以及p53蛋白过表达情况，以研究它们是否代表相似或不同的癌症分子途径。在散发性腺瘤中，32%的病例检测到K-ras突变，31%的病例检测到p53过表达。同样，25%的HNPCC腺瘤中同时发现了K-ras突变和p53过表达。HNPCC和散发性腺瘤中这些异常的频率没有显著差异。考虑到腺瘤大小的差异，频率更加相似。总之，这些结果表明，就K-ras和p53的参与情况而言，HNPCC和散发性癌变中腺瘤的分子途径相似。
