Mutational Analysis of Proapoptotic Bcl-2 Family Members in Gastric Carcinomas

위암에서의 고사유발성 Bcl-2 Family의 돌연변이에 관한 연구

  • Yoo Nam Jin (Department of Pathology, College of Medicine, The Catholic University of Korea) ;
  • Lee Jong Woo (Department of Pathology, College of Medicine, The Catholic University of Korea) ;
  • Soung Young Hwa (Department of Pathology, College of Medicine, The Catholic University of Korea) ;
  • Kim Hong Sug (Department of Pathology, College of Medicine, The Catholic University of Korea) ;
  • Park Won Sang (Department of Pathology, College of Medicine, The Catholic University of Korea) ;
  • Lee Jung Young (Department of Pathology, College of Medicine, The Catholic University of Korea) ;
  • Lee Sug Hyung (Department of Pathology, College of Medicine, The Catholic University of Korea)
  • 유남진 (가톨릭대학교 의과대학 병리학교실) ;
  • 이종우 (가톨릭대학교 의과대학 병리학교실) ;
  • 송영화 (가톨릭대학교 의과대학 병리학교실) ;
  • 김홍석 (가톨릭대학교 의과대학 병리학교실) ;
  • 박원상 (가톨릭대학교 의과대학 병리학교실) ;
  • 이정용 (가톨릭대학교 의과대학 병리학교실) ;
  • 이석형 (가톨릭대학교 의과대학 병리학교실)
  • Published : 2003.06.01

Abstract

Purpose: Evidence exists that dysregulation of Bcl-2 family members is involved in the pathogenesis of cancer development. The aim of this study was to explore whether the somatic mutation of proapoptotic Bcl-2 member genes, one of the mechanisms that prolong the survival of cancer cells, is involved in gastric carcinogenesis. Materials and Methods: In the current study, to detect somatic mutations of the DNA sequences encoding the Bcl-2 homology 3 (BH3) domain of the human BAD, BIM, BIK, and Bcl-G genes in 60 advanced gastric adenocarcinomas, we used the polymerase chain reaction (PCR), single strand conformation polymorphism (SSCP), and DNA sequencing. Results: The SSCP analysis revealed no mutations in the coding regions of the BH3 domain in the cancers. Conclusion: The data presented here indicate that proapoptotic Bcl-2 member genes, BAD, BIM, BIK, and Bcl-G, may not be mutated in human gastric carcinomas and suggest that these genes might be altered by mechanisms other mechanisms somatic mutation.

Keywords