Alterations and hypermethylation of the p14ARF gene in gastric cancer
作者： Satoru Iida , Yoshimitsu Akiyama , Tomoko Nakajima , Wataru Ichikawa , Zenro Nihei
DOI: 10.1002/1097-0215(20000901)87:5<654::AID-IJC6>3.0.CO;2-P
关键词: Methylation 、 Biology 、 Molecular biology 、 Mutation 、 Cancer research 、 p14arf 、 Promoter 、 Cancer 、 Tumor suppressor gene 、 Exon 、 DNA methylation
摘要: p14(ARF), generated through an alternative splicing process that replaces the first exon, 1alpha, of p16(INK4a) with exon 1beta, located >15 kb upstream has been shown to function as a growth suppressor. We examined 11 gastric cancer cell lines for mRNA expression, homozygous deletion, mutation, and promoter methylation p14(ARF) gene. No expression was detected in 5 7 diffuse-type lines. All intestinal displayed normal levels except one low level expression. Of without 3 (MKN45, NUGC-2, NUGC-4) 1 (KATO III) deletion gene, respectively. mutation found whole coding region gene 8 deletion. Our results indicate is more frequently inactivated by or (5/7, 71.4%) than ones (0/4, P = 0.022). When we also analyzed 62 primary cancers status region, frequency tended be higher (15/33, 45.5%) (7/28, 25%). Thus, alterations might involved carcinogenesis.
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