Korean J Gastroenterol.
2007 Apr;49(4):209-224.
Gene Expression Profiling using Oligonucleotide Microarray in Atrophic Gastritis and Intestinal Metaplasia
- Affiliations
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- 1Department of General Surgery, Konkuk University College of Medicine, Chungju, Korea. kkongr@kku.ac.kr
- 2Department of Internal Medicine, Konkuk University College of Medicine, Chungju, Korea.
- 3Department of Family Medicine, Konkuk University College of Medicine, Chungju, Korea.
- 4Department of Pathology, Konkuk University College of Medicine, Chungju, Korea.
- 5Department of Anatomy, Konkuk University College of Medicine, Chungju, Korea.
- 6Department of Biotechnology, College of Biomedical and Health Science, Chungju, Korea.
- 7Department of Internal Medicine, Busan St. Mary's Hospital, Busan, Korea.
Abstract
- BACKGROUND/AIMS
The atrophic gastritis with intestinal metaplasia of gastric mucosa has been considered to be the major factor of carcinogenesis in the stomach. However, the key molecules are still poorly understood. To elucidate the molecular genetic basis, we report the results of our initial microarray data to analyze the genome pattern in patients with atrophic gastritis and intestinal metaplasia of the stomach.
METHODS
We used oligonucleotide microarray technique to evaluate the gene expression profiles in atrophic gastritis with intestinal metaplasia, in comparison with those of normal mucosa. For the identification of differentially expressed genes, Significance Analysis of Microarrays (SAM) package method was used. The results were analyzed using global normalization, intensity dependent normalization, and box plot normalization.
RESULTS
Eight genes including FABP, REG, OR6C1, MEP1, SLC6A1, SI, Mucin 1, and RAB23 in mucosa of atrophic gastritis and intestinal metaplasia were up-regulated by more than 10 times as compared with normal gastric mucosa. Only one gene, LOC44119 was down-regulated by more than 10 times of the expression as compared with normal gastric mucosa. In respect to the expression of known genes related to gastric carcinogenesis, 8 genes including FN1, SRMS, TP53, TP53IMP2, TP53I3, FGFR4, TGFB1, and TGFA showed up- and down-regulations more than 2 folds in expression pattern.
CONCLUSIONS
We could identify a total genome pattern in patient with atrophic gastritis and intestinal metaplasia using oligonucleotide microarray. We believe that the current results will serve as a fundamental bioinformative basis for clinical applications in diagnosis and treatment of gastric cancer and precancerous lesion in the future.
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