Mutational Analysis of the Epidermal Growth Factor Receptor Gene in Gastrointestinal Stromal Tumors.
10.5230/jkgca.2004.4.4.268
- Author:
Nam Jin YOO
1
;
Jong Woo LEE
;
Young Hwa SOUNG
;
Hae Myung JEON
;
Suk Woo NAM
;
Su Young KIM
;
Won Sang PARK
;
Jung Young LEE
;
Sug Hyung LEE
Author Information
1. Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, Korea. suhulee@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Epidermal growth factor receptor gene;
Gastrointestinal stromal tumor;
Mutation
- MeSH:
Epidermal Growth Factor*;
Exons;
Gastrointestinal Stromal Tumors*;
Genes, erbB-1;
Humans;
Phosphotransferases;
Polymerase Chain Reaction;
Polymorphism, Single-Stranded Conformational;
Receptor, Epidermal Growth Factor*;
Receptors, Platelet-Derived Growth Factor;
Sequence Analysis, DNA
- From:Journal of the Korean Gastric Cancer Association
2004;4(4):268-271
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PUPOSE: Most gastrointestinal stromal tumors (GISTs) have gain-of-function mutations of the KIT or the platelet-derived growth factor receptor alpha (PDGFRA) genes, but approximately 10% of the GISTs are wild types for both the KIT and the PDGFRA genes. The purpose of this study was to investigate the possibility that epidermal growth factor receptor (EGFR) gene mutation might be responsible for the pathogenesis of GIST. MATERIALS AND METHODS: We analyzed the EGFR gene in 60 GISTs for the detection of somatic mutations by using the polymerase chain reaction (PCR), the single strand conformation polymorphism (SSCP), and DNA sequencing in exon 18, 19, and 21 encoding the kinase domain. RESULTS: The SSCP analysis revealed no evidence of EGFR mutations in exon 18, 19, and 21 in GISTs. CONCLUSION: The data indicate that the EGFR gene may not be mutated in human GIST and suggest that therapies targeting the mutated EGFR gene products might not be useful in the treatment of GISTs.
