Premium
Immunohistochemical analysis of phospho‐BAD protein and mutational analysis of BAD gene in gastric carcinomas
Author(s) -
JEONG EUN GOO,
LEE SUNG HAK,
KIM SUNG SOO,
AHN CHANG HYEOK,
YOO NAM JIN,
LEE SUG HYUNG
Publication year - 2007
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1600-0463.2007.apm_804.x
Subject(s) - carcinogenesis , immunohistochemistry , biology , single strand conformation polymorphism , gene , mutation , cancer , apoptosis , cancer research , somatic cell , germline mutation , gene mutation , gene expression , microbiology and biotechnology , genetics , immunology
Mounting evidence indicates that deregulation of apoptosis contributes to the development of human cancers. BAD, a proapoptotic Bcl‐2 family protein, regulates the intrinsic apoptosis pathway. The aim of this study was to explore whether alterations of phospho‐BAD (p‐BAD) protein that antagonizes apoptosis function of BAD and mutation of BAD gene are characteristics of human gastric cancers. We analyzed expression of p‐BAD in 60 gastric adenocarcinomas by immunohistochemistry. Also, we analyzed BAD gene for detection of somatic mutations by single‐strand conformation polymorphism (SSCP) assay. p‐BAD expression was detected well in normal gastric mucosal epithelial cells, whereas it was detected in only 51% (31 of the 60) of the cancers. There was no somatic mutation of BAD gene in the 60 gastric cancer samples. The decreased expression of p‐BAD in malignant gastric epithelial cells compared to normal mucosal epithelial cells suggested that loss of p‐BAD expression may play a role in gastric tumorigenesis. The data also suggest that BAD mutation may not be a direct target of inactivation in gastric tumorigenesis.