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K‐ ras mutation in h elicobacter pylori ‐associated chronic gastritis in patients with and without gastric cancer
Author(s) -
Hiyama Toru,
Haruma Ken,
Kitadai Yasuhiko,
Masuda Hiroshi,
Miyamoto Masaki,
Tanaka Shinji,
Yoshihara Masaharu,
Shimamoto Fumio,
Chayama Kazuaki
Publication year - 2001
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.1644
Subject(s) - helicobacter pylori , cancer , carcinogenesis , chronic gastritis , gastritis , gastroenterology , medicine , mutation , oncogene , stomach cancer , biology , cancer research , gene , genetics , cell cycle
Mutations of an oncogene, K‐ ras , are associated with the development and progression of many types of human cancer. To elucidate the significance of K‐ ras mutations in gastric carcinogenesis, we examined K‐ ras mutations in gastric cancers and in Helicobacter pylori ‐associated chronic gastritis ( H. pylori ‐ CG), which is associated with an increased risk for the gastric cancer development. Specimens of gastric cancer and H. pylori ‐ CG were obtained from 64 gastric cancer patients with H. pylori ‐CG, 99 cancer‐free H. pylori ‐CG patients and 30 H. pylori ‐negative healthy subjects. K‐ ras mutations were examined by polymerase chain reaction‐single strand conformation polymorphism (PCR‐SSCP), followed by DNA sequencing analysis. K‐ ras mutations were detected in 4 of 48 (8.3%) gastric cancers, in 10 of 163 (6.1%) H. pylori ‐CG and none of the 30 H. pylori ‐negative healthy subjects. In the gastric cancer patients, mutated K‐ ras was detected in differentiated type cancers but not in any of the undifferentiated type cancers. K‐ ras mutations in H. pylori ‐CG were significantly more frequent in gastric cancer patients than in cancer‐free patients (10.9% vs. 3.0%, p = 0.044). In addition, K‐ ras mutations in H. pylori ‐CG were significantly more frequent in patients with K‐ ras mutated gastric cancer than in patients with K‐ ras unmutated gastric cancer (50.0% vs. 3.7%, p = 0.037). These data suggest that the genetic mechanism(s) of carcinogenesis differs between the differentiated type and the undifferentiated type of gastric cancer and that K‐ ras mutations may be involved in the early stages of gastric carcinogenesis of the differentiated type. © 2001 Wiley‐Liss, Inc.