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Alterations of BAT-26 identify a subset of gastric cancer with distinct clinicopathologic features and better postoperative 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.