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K-ras activation in gastric epithelial tumors in Japanese
H Miki1, M Ohmori, A O Perantoni
1Department of Pathology, Kagawa Medical School, Japan.
Abstract:
Point mutation in codons 12, 13 and 61 of the K-ras oncogene in gastric epithelial tumors were investigated by polymerase chain reaction from sections of formalin-fixed, paraffin-embedded tissue followed by dot-blot hybridization with mutation-specific oligonucleotide probes. Point mutations were found specifically in four of 20 tumors of intestinal histological subtype; GGT to GAT in three cases and to GTT in one case, all in codon 12 of K-ras. These mutations were also confirmed by direct sequencing. In contrast, none of 11 diffuse-type tumors showed K-ras point mutations. While K-ras point mutations may not be frequent events in gastric tumorigenesis, the similarity of the intestinal-type gastric tumors and colorectal tumors for K-ras point mutations as well as the association of mutations in K-ras with a particular gastric tumor histology implicates K-ras activation in the development of these tumors.
Insights
Point mutations in the K-ras oncogene were identified in intestinal-type gastric tumors but not in diffuse-type tumors. This finding suggests K-ras activation plays a role in specific gastric cancer development.
Area of Science:
- Oncology
- Molecular Biology
- Gastroenterology
Background:
- The K-ras oncogene is frequently mutated in various cancers, including colorectal cancer.
- Gastric cancer exhibits diverse histological subtypes with distinct molecular profiles.
- The role of K-ras mutations in gastric tumorigenesis remains incompletely understood.
Purpose of the Study:
- To investigate the presence and significance of point mutations in codons 12, 13, and 61 of the K-ras oncogene in gastric epithelial tumors.
- To correlate K-ras mutations with specific histological subtypes of gastric cancer.
Main Methods:
- Polymerase chain reaction (PCR) was used to analyze DNA from formalin-fixed, paraffin-embedded gastric tumor tissues.
- Dot-blot hybridization with mutation-specific oligonucleotide probes identified K-ras mutations.
- Direct sequencing confirmed the identified mutations.
Main Results:
- Point mutations in K-ras codon 12 (GGT to GAT or GTT) were detected in 4 out of 20 intestinal-type gastric tumors.
- No K-ras point mutations were found in 11 diffuse-type gastric tumors.
- The observed mutations were confirmed by direct sequencing.
Conclusions:
- K-ras point mutations are associated with the intestinal histological subtype of gastric cancer.
- The findings suggest a role for K-ras activation in the development of intestinal-type gastric tumors.
- The molecular similarities in K-ras mutations between intestinal-type gastric and colorectal tumors warrant further investigation.