科研之友
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摘要
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%26apos; 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.
