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J Korean Gastric Cancer Assoc. 2003 Jun;3(2):84-87. Korean. Original Article. https://doi.org/10.5230/jkgca.2003.3.2.84
Yoo NJ , Lee JW , Soung YH , Kim HS , Park WS , Lee JY , Lee SH .
Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, Korea. suhulee@catholic.ac.kr
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.

Copyright © 2019. Korean Association of Medical Journal Editors.