Analysis of K-ras codon 12 mutations and p53 overexpression in colorectal nodule-aggregating tumors
Article first published online: 7 JUL 2008
Journal of Gastroenterology and Hepatology
Volume 15, Issue 10, pages 1151–1157, October 2000
How to Cite
Kusaka, T., Fukui, H., Ueda, Y., Chiba, T. and Fujimori, T. (2000), Analysis of K-ras codon 12 mutations and p53 overexpression in colorectal nodule-aggregating tumors. Journal of Gastroenterology and Hepatology, 15: 1151–1157. doi: 10.1046/j.1440-1746.2000.02280.x
- Issue published online: 7 JUL 2008
- Article first published online: 7 JUL 2008
- adenoma–carcinoma sequence;
- colorectal tumor;
- polypoid growth
Abstract Background and Aims: Morphologically, colorectal nodule-aggregating tumors are quite different from polypoid-type colorectal tumors that develop via the adenoma–carcinoma sequence. Although polypoid-type colorectal tumors are well known to have a high incidence of K-ras gene mutation and p53 overexpression, colorectal nodule-aggregating tumors have not been examined in terms of genetic changes and clinicopathological features. In the present study, therefore, we analysed the clinicopathological features, genetic changes in K-ras codon 12, and p53 overexpression in colorectal nodule-aggregating tumors.
Methods: A total of 18 colorectal nodule-aggregating tumors were surgically resected and then analysed clinicopathologically. Immunohistochemistry and polymerase chain reaction–single stranded conformational polymorphism were performed to analyse p53 abnormalities in the tumors. K-ras codon 12 mutations were screened out by the polymerase chain reaction–restriction fragment length polymorphism method and analysed by fluorescence direct sequencing.
Results: p53 overexpression was observed in six lesions (33%). p53-overexpressing cells were observed in parts of carcinoma or adenoma showing high-grade atypia. Four of the 10 (40%) samples had a p53 gene mutation. Nine of the 18 (50%) samples had a K-ras codon 12 point mutation. In eight cases (89%), the mutations of the K-ras codon 12 were of the same type: GGT (glycine) to GTT (valine).
Conclusions: The colorectal nodule-aggregating tumor has distinctive characteristics showing a morphological phenotype of the superficial-type tumors and genotype of the polypoid tumors in terms of K-ras gene mutation and p53 overexpression.