Gene Expression Profiling using Oligonucleotide Microarray in Atrophic Gastritis and Intestinal Metaplasia.
- Author:
Kyong Rae KIM
1
;
Soo Youn OH
;
Ung Chae PARK
;
Joon Ho WANG
;
Jae Dong LEE
;
Hyuk Jung KWEON
;
Sang Yoon KIM
;
Seung Hwa PARK
;
Dong Kug CHOI
;
Chan Gil KIM
;
Seongc Ho CHOI
Author Information
1. Department of General Surgery, Konkuk University College of Medicine, Chungju, Korea. kkongr@kku.ac.kr
- Publication Type:Original Article ; English Abstract
- Keywords:
Gastric cancer;
Atrophic gastritis;
Intestinal metaplasia;
Oligonucleotide microarray;
Gene expression
- MeSH:
Down-Regulation;
Gastritis, Atrophic/*genetics/metabolism;
Gene Expression Profiling;
Humans;
Intestines/*metabolism/*pathology;
Metaplasia/genetics/metabolism;
Microarray Analysis;
Tumor Markers, Biological/genetics/metabolism;
Up-Regulation
- From:The Korean Journal of Gastroenterology
2007;49(4):209-224
- CountryRepublic of Korea
- Language:Korean
-
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.
