BACKGROUND/AIMS: Gastrointestinal tumors with microsatellite instability represent a replication error-positive phenotype. BAT-26, a repeat of 26 deoxyadenosine localized in intron 5 of hMSH2 gene, has been reported as a reliable indicator of replication error phenotype in colorectal cancers. This study investigated whether BAT-26 is a useful marker for a mutator phenotype with distinct clinicopathologic features in gastric cancer. METHODOLOGY: One hundred and nineteen gastric cancer tissues and matched non-tumor tissue were examined by polymerase chain reactions with electrophoresis for 9 dinucleotide microsatellites and BAT-26, and frameshift mutations of transforming growth factor-beta type II receptor. The relation between BAT-26 alterations and relevant clinicopathological or genetic parameters were analyzed. RESULTS: Gastric cancer with BAT-26 alterations was highly correlated with multiple microsatellite alterations (> or = 3 loci) and frameshift mutations of transforming growth factor-beta type II receptor, and predominantly showed antral location, intestinal histologic subtype, advanced stage, a higher rate of Helicobacter pylori infection, a better postoperative survival and less lymph node metastasis. CONCLUSIONS: These results show testing of BAT-26 alterations is a convenient and rapid screening method for identifying a subset of gastric cancer with a mutator phenotype and better prognosis.
BACKGROUND/AIMS: Gastrointestinal tumors with microsatellite instability represent a replication error-positive phenotype. BAT-26, a repeat of 26 deoxyadenosine localized in intron 5 of hMSH2 gene, has been reported as a reliable indicator of replication error phenotype in colorectal cancers. This study investigated whether BAT-26 is a useful marker for a mutator phenotype with distinct clinicopathologic features in gastric cancer. METHODOLOGY: One hundred and nineteen gastric cancer tissues and matched non-tumor tissue were examined by polymerase chain reactions with electrophoresis for 9 dinucleotide microsatellites and BAT-26, and frameshift mutations of transforming growth factor-beta type II receptor. The relation between BAT-26 alterations and relevant clinicopathological or genetic parameters were analyzed. RESULTS:Gastric cancer with BAT-26 alterations was highly correlated with multiple microsatellite alterations (> or = 3 loci) and frameshift mutations of transforming growth factor-beta type II receptor, and predominantly showed antral location, intestinal histologic subtype, advanced stage, a higher rate of Helicobacter pylori infection, a better postoperative survival and less lymph node metastasis. CONCLUSIONS: These results show testing of BAT-26 alterations is a convenient and rapid screening method for identifying a subset of gastric cancer with a mutator phenotype and better prognosis.
Authors: Won Hyuk Choe; Sun-Young Lee; Jun Haeng Lee; Sang Goon Shim; Young-Ho Kim; Poong-Lyul Rhee; Jong Chul Rhee; Chang-Seok Ki; Jong-Won Kim; Sang Yong Song; Jae J Kim Journal: Korean J Intern Med Date: 2005-06 Impact factor: 2.884
Authors: Paulo Figueiredo; Maximino Leitão; Célia Nogueira; Marta Mota; Rui Gradiz; Maria Augusta Cipriano; Francisco Caramelo; Hugo Cruz; Ana Alarcão; Francisco Castro E Sousa; Fernando Oliveira; Fernando Martinho; João Moura Pereira Journal: Infect Agent Cancer Date: 2017-07-19 Impact factor: 2.965