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Background/aims: p53 gene plays an important role in cell cycle control in response to DNA damage which may increase the probability of mutations leading to carcinogenesis. The role of p53 gene polymorphisms [codon 72 (exon 4) and 16-bp duplication (intron 3)] as potential markers indicating cancer risk remains inconclusive, and the data on gastric cancer are very limited. The aim of this study was to assess the role of p53 gene polymorphisms in the risk of gastric cancer and in the determination of genetic susceptibility to gastric cancer in Koreans., Methods: We analysed p53 genotypes using a polymerase chain reaction-based restriction fragment length polymorphism assay in a population-based case-control study in 120 gastric cancer patients and 145 cancer-free controls in Koreans., Results: There was no specific genotype of p53 gene polymorphism in the gastric cancer patients compared to cancer-free controls. In p53 codon 72 and 16-bp duplication polymorphisms, the frequency and distribution of genotypes showed no statistical significance (p=0.7125 and p=0.1659). There was no difference in genotype by histologic subtypes, location of lesion, and age. However, the genotypic distribution in the patient subgroups with a history of heavy cigarette smoking of p53 16-bp duplication polymorphism were significantly different from those of cancer-free controls (p=0.0079)., Conclusions: The p53 codon 72 and 16-bp duplication polymorphisms were not associated with the increased risk of gastric cancer and did not seem to contribute to gastric cancer susceptibility among Koreans. It is possible that p53 16-bp duplication polymorphism modulates the risk of smoking-induced gastric cancer development in Koreans. In order to clarify the associations between specific genotypes and gastric cancer risk, the evaluations of these polymorphisms in other ethnic backgrounds with larger number of patients would be needed.

Background: fms-like tyrosine kinase (FLT3), a member of the class III receptor tyrosine kinases, regulates the proliferation and differentiation of hematopoietic stem cells. An internal tandem duplication of the FLT3 gene (FLT3/ITD) has been reported in acute myelogenous leukemia (AML) and may be associated with a poor prognosis. In this study we determined the prevalence and prognostic significance of FLT3/ITD in adult AML patients., Methods: This study included 52 adult de novo AML. Exon 14 and 15 of the FLT3 gene were amplified by PCR and the PCR products were analyzed by 3730XL DNA analyzer (Applied Biosystems, USA) and GeneMapper Software., Results: FLT3/ITD was found in 15 (28.8%) of the 52 AML patients. The presence of FLT3/ITD was significantly associated with absolute leukocyte counts (P=0.002) and bone marrow blast counts (P=0.036). FLT3/ITD was also more frequent in patients with normal karyotype (7 of 18) than in those with cytogenetic aberrations (3 of 25). Patients with t (15;17) showed a higher prevalence of FLT3/ITD (2 of 7). FLT3/ITD was significantly associated with overall survival (P<0.042)., Conclusions: Our data indicate that FLT3/ITD is a common alteration in adult AML patients. Although based on a study with a limited number of AML patients, FLT3/ITD is a prognostic marker in patients with AML.