p53 expression, K-ras gene mutation and microsatellite instability in gastric B-cell lymphomas

Background and Aims: Genetic mechanisms involved in the development of gastric B‐cell lymphomas remain unclear. The aim of the present study was to clarify the roles of mutations of the p53 and K‐ras genes, and microsatellite instability (MSI) in the development of gastric B‐cell lymphomas. Methods: We investigated p53 immunoreactivity, mutations of the K‐ras gene, and MSI in 27 gastric marginal zone B‐cell lymphomas of mucosa‐associated lymphoid tissue type (MZBCL) and 24 diffuse large B‐cell lymphomas (DLBCL). p53 immunoreactivity was examined using a monoclonal antibody, DO‐7. Mutation of the K‐ras gene was detected by polymerase chain reaction‐single strand conformation polymorphism (PCR‐SSCP) analysis. MSI was examined at five microsatellite loci with a microsatellite assay. Cases were classified as having high‐frequency MSI (MSI‐H) (≥ 2 loci showing instability), low‐frequency MSI (MSI‐L) (only one locus showing instability), or as microsatellite stable. Results: p53 immunoreactivity was detected in 1 of 16 (6%) MZBCL and 8 of 19 (42%) DLBCL. Frequency of p53 immunoreactivity in DLBCL was significantly higher than that in MZBCL (P = 0.018). MSI‐H was detected only in 1 of 20 (5%) DLBCL. None of the cases examined showed mutation of the K‐ras gene. Conclusions: These data suggest that mutations of the p53 gene may play an important role in the development of gastric DLBCL, and that mutations of the K‐ras gene and MSI may be involved in little part of the development of gastric B‐cell lymphomas.