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Analysis of K‐ ras codon 12 mutations and p53 overexpression in colorectal nodule‐aggregating tumors
Author(s) -
Kusaka Toshihiro,
Fukui Hirokazu,
Ueda Yoshihiko,
Chiba Tsutomu,
Fujimori Takahiro
Publication year - 2000
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.2000.02280.x
Subject(s) - point mutation , mutation , adenoma , pathology , colorectal cancer , nodule (geology) , atypia , gene mutation , genotype , cancer research , gene , colorectal adenoma , biology , medicine , microbiology and biotechnology , cancer , genetics , paleontology
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.