Kim Sang-Pyo, Hwang Mi-Sun, Cho Young Rok, Kwon Sun Young, Kang Yu-Na, Kim In-Ho, Sohn Soo-Sang, Mun Kyo-Cheol, Kwon Taeg-Kyu, Lee Seong-Ryong, Suh Seong-Il
Department of Pathology, School of Medicine, Keimyung University, #194 DongSan Dong Jung-Gu, 700-712 Daegu, South Korea.
Cancer Lett. 2003 May 30;195(1):87-91. doi: 10.1016/s0304-3835(02)00585-2.
The bcl-2 homologue antagonist/killer (BAK) is a potently apoptosis-inducing gene and plays an important role in modulating apoptosis in epithelial cells. We have analyzed the mutation of the entire coding region of BAK gene in 107 Korean advanced gastric adenocarcinomas by polymerase chain reaction-single strand conformation polymorphism and sequencing. Homozygous deletions were not found in these samples. Only three cases of 107 gastric adenocarcinomas (2.8%) exhibited the BAK mutations. Two of them exhibited missense mutations and the remaining one had a silent mutation. All of these mutations were exclusively detected in exon 2. Mutations in the BAK gene were observed only in advanced gastric adenocarcinomas with extensive metastases of regional lymph nodes. The data presented here suggest that the mutations of BAK gene rarely occurred in advanced gastric adenocarcinomas.
bcl-2同源拮抗剂/杀手（BAK）是一种强效的凋亡诱导基因，在调节上皮细胞凋亡中起重要作用。我们通过聚合酶链反应-单链构象多态性和测序分析了107例韩国晚期胃腺癌中BAK基因整个编码区的突变情况。在这些样本中未发现纯合缺失。107例胃腺癌中仅有3例（2.8%）出现BAK突变。其中2例表现为错义突变，其余1例为沉默突变。所有这些突变均仅在外显子2中检测到。BAK基因突变仅在伴有区域淋巴结广泛转移的晚期胃腺癌中观察到。此处呈现的数据表明，BAK基因的突变在晚期胃腺癌中很少发生。
