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Analysis of Ki‐ras and p53 gene mutations in laterally spreading tumors of the colorectum
Author(s) -
Noro Akihiro,
Sugai Tamotsu,
Habano Wataru,
Nakamura Shinichi
Publication year - 2003
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1046/j.1440-1827.2003.01564.x
Subject(s) - pathology , gene , biology , cancer research , medicine , genetics
A laterally spreading tumor (LST) is considered to be a specific subtype of superficial colorectal tumors, in view of its characteristic clinicopathological features. We attempted to compare genetic alterations found in LST (>10 mm) with those found in IIa‐type adenomas (10 mm or less (small superficial elevated lesion)) and conventional polypoid adenomas (>10 mm). In addition, multiple sampling by microdissection was performed for 14 LST to examine genetic heterogeneity in the Ki‐ras and p53 gene mutation patterns. Polymerase chain reaction, single‐strand conformation polymorphism and direct sequencing were used to analyze Ki‐ras and p53 gene mutations in 73 sporadic colorectal adenomas: 28 LST; 22 IIa‐type adenomas; and 23 polypoid adenomas. Ki‐ras gene mutations were found more frequently in LST (6/28 tumors) and polypoid adenomas (6/23 tumors) than in IIa‐type adenomas (2/22 tumors), although this difference was not statistically significant. The frequency of p53 gene mutations in the 28 LST was 25% (7/28), which was significantly higher than that found in IIa‐type adenomas ( P  < 0.05). However, although p53 gene mutations were found more frequently in LST than in polypoid adenomas, this difference was not statistically significant. Seven LST exhibited a combination of wild‐type and mutant‐type tumor cells having the p53 gene mutation pattern, whereas a pattern of different Ki‐ras gene mutations was found in two of three LST that exhibited Ki‐ras gene mutation heterogeneity. We suggest that the LST exhibited a characteristic pattern in terms of the Ki‐ras as well as the p53 gene mutation pattern, thereby supporting the hypothesis that LST is a specific subtype of colorectal tumors.

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