作者: M. Anne-Marie Aguelon , Nikolai M. Mironov , Hiroshi Yamasaki , Yasufumi Omori , Oleg V. Gorbunov
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摘要: We have examined whether alterations of simple (CA)n DNA repeats, as observed in human colon cancers, occur during gastric carcinogenesis and such reflect genomic instability that could lead to other genetic changes. A total 22 cancer samples were analyzed: 15 well or moderately differentiated adenocarcinomas, 6 signetring cell carcinomas, 1 poorly adenocarcinoma. When repeat sequences at 10 loci, one adenocarcinoma showed a loss five three adenocarcinomas gained locus, had new, repeated loci. Three mutations the p53 gene, two exon 5 (both GC AT transition CpG dinucleotide) 7 (AT transition). Only sample with mutation also altered repeats. putative tumor suppressor connexin 32, was not assessed by single-strand conformation polymorphism analysis. These results suggest revealed changes does seem contribute induction point 32 genes but may participate heterozygosity APC/MCC The are consistent hypothesis different mechanisms involved gain