Belyavskaya V.A.,Vector State Center for Research in Virusology and Biotechnology |
Vardosanidze K.V.,Municipal Oncological Dispensary |
Oreshkova S.F.,Vector State Center for Research in Virusology and Biotechnology |
Blinov A.G.,RAS Institute of Cytology and Genetics |
And 4 more authors.
Voprosy Onkologii | Year: 2010
The paper deals with a study of p53 gene somatic mutations in tumor cell genomes from patients with stomach cancers of different histological patterns. It used sequential and molecular cloning methods. The former involved amplicones characterized by abnormal volatility following SSCP analysis of plasmids from 9 tumors. Replacement nucleotides were identified in 4 tumors (intestinal - 2, diffuse - 2). Among 8 mutations were 1 single-nucleotide deletion in codon-249 with shifting sensing frame and one targeted mutation. Five of the former were missens-mutations which caused amino acid replacement while the other two silent mutations did not. Exon-assisted analysis of p53 («wild») gene identified cells with stable structure in each tumor (1 mutation - 2; 3 mutations - 2 including genuinely-paired mutations in 1 exon). All mutations occurred in structurally and functionally important codons. Our evidence corroborated earlier data of SSCP analysis on tumor cell presence in populations with variable p53 genomes. Source