Journal of Gastric Cancer

  • 제4권4호
  • /
  • Pages.268-271
  • /
  • 2004
  • /
  • 2093-582X(pISSN)
  • /
  • 2093-5641(eISSN)
대한위암학회 (The Korean Gastric Cancer Association)
권호 표지

위장관 간질성 종양의 Epidermal Growth Factor Receptor 유전자 돌연변이 연구

Mutational Analysis of the Epidermal Growth Factor Receptor Gene in Gastrointestinal Stromal Tumors

  • 유남진 (가톨릭대학교 의과대학 병리학교실) ;
  • 이종우 (가톨릭대학교 의과대학 병리학교실) ;
  • 송영화 (가톨릭대학교 의과대학 병리학교실) ;
  • 전해명 (가톨릭대학교 의과대학 외과학교실) ;
  • 남석우 (가톨릭대학교 의과대학 병리학교실) ;
  • 김수영 (가톨릭대학교 의과대학 병리학교실) ;
  • 박원상 (가톨릭대학교 의과대학 병리학교실) ;
  • 이정용 (가톨릭대학교 의과대학 병리학교실) ;
  • 이석형 (가톨릭대학교 의과대학 병리학교실)
  • Yoo Nam Jin (Departments of Pathology College of Medicine, The Catholic University of Korea) ;
  • Lee Jong Woo (Departments of Pathology College of Medicine, The Catholic University of Korea) ;
  • Soung Young Hwa (Departments of Pathology College of Medicine, The Catholic University of Korea) ;
  • Jeon Hae Myung (Departments of General Surgery, College of Medicine, The Catholic University of Korea) ;
  • Nam Suk Woo (Departments of Pathology College of Medicine, The Catholic University of Korea) ;
  • Kim Su Young (Departments of Pathology College of Medicine, The Catholic University of Korea) ;
  • Park Won Sang (Departments of Pathology College of Medicine, The Catholic University of Korea) ;
  • Lee Jung Young (Departments of Pathology College of Medicine, The Catholic University of Korea) ;
  • Lee Sug Hyung (Departments of Pathology College of Medicine, The Catholic University of Korea)
  • 발행 : 2004.12.01
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초록

Purpose: 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.

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