Abnormal Fragile Histidine Triad Gene Expression in Gastric Cancer.
10.5230/jkgca.2003.3.1.26
- Author:
Moon Soo LEE
1
;
Tae Yun KIM
;
Gyu Seok CHO
;
Man Kyu CHAE
;
Sung Yong KIM
;
Moo Jun BAEK
;
Sang Han LEE
;
Kyung Kyu PARK
;
Chang Ho KIM
;
Ok Pyung SONG
;
Moo Sik CHO
Author Information
1. Department of Surgery, College of Medicine, Soonchunhyatng University, Chunan, Korea. hychung@knu.ac.kr
- Publication Type:Original Article
- Keywords:
Gastric cancer;
FHIT
- MeSH:
Carcinogenesis;
DNA;
Gene Expression*;
Histidine*;
Loss of Heterozygosity;
RNA;
Stomach Neoplasms*
- From:Journal of the Korean Gastric Cancer Association
2003;3(1):26-32
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Genomic alterations and abnormal expression of the fragile histidine triad (FHIT) gene in gastric cancer were examined to determine whether the FHIT gene is actually a frequent target for alteration during gastric carcinogenesis. MATENRIALS AND METHODS: To correlate DNA and RNA lesions of the FHIT gene with the effect on FHIT protein expression, in 40 gastric cancers, we investigated the FHIT gene for loss of heterozygisity (LOH), aberrant transcripts, and protein expression. RESULTS: Allelic loss at D3S1300 was detected in 7 of 38 (19%) informative cases. Aberrant transcripts were observed in 20 of 40 (50%) cases. Significant reduction of FHIT protein expression was observed in 22 of 40 (55%) cases. Aberrant FHIT transcription was shown to be associated with loss of FHIT protein expression. However, aberrent FHIT transcripts themselves were not associated with any clinicopathological parameters, such as age, sex, tumor site, or clinical stage. Moreover, there was no association between the presence of LOH at D3S1300 and the expression of aberrant FHIT transcripts. CONCLUSION: The high frequency of aberrant FHIT transcripts, the significant rate of LOH at D3S1300, and the altered expression of the FHIT protein indicate that alterations of the FHIT gene can play an important role in gastric carcinogenesis.
