INTRODUCTION: Primary gastric lymphomas account for 50% of the extranodal non-Hodgkin lymphoma and for 2% to 8% of the malignant gastric neoplasms. Most of them arise from B lymphocytes proliferation of the mucosaassociated lymphoid tissue. This tissue is not present in stomach in normal conditions; it arises secondarily to chronic gastritis, frequently associated to the bacterium Helicobacter pylori. Chronic inflammation of the bacterium infection seems to induce T lymphocytes, leading to persistent stimulation of B lymphocytes that initially proliferate in a reactive fashion. After that, there are some genomic changes in the lymphoid cells, including BCL-2 and BCL-6 mutation inducing some proliferating gain, clonal selection and neoplastic transformation, originating the lowgrade gastric lymphoma. Additional genetic changes, like p53 mutation, can induce high-grade transformation. MATERIAL AND METHODS: We revised 32 cases of gastric lymphomas: 15 low and 17 high-grade. The age and the gender of those patients were investigated. The morphological characteristics of the lesions and Helicobacter pylori colonization were assessed. Immunohistochemistry to CD20, Ki-67, p53, BCL-2 and BCL-6 was performed. RESULTS: Gastric lymphomas occur more frequently in males and patients' age is more advanced in the low grade group. Lymphoepithelial lesions were observed in 93% of this lymphoma group. The proliferative rate and p53 expression were greater in the high grade group. The BCL-2 expression was higher in the low grade lymphoma group. There were no significant differences in BCL-6 expression in both groups. CONCLUSION: The results suggest that genes P53 and BCL-2 play a role in the pathogenesis and evolution of gastric lymphomas.
Gastric lymphoma; MALT; p53; BCL-2; BCL-6; Immunohistochemistry
