Genetic and epigenetic factors involved in B‐cell lymphomagenesis

Malignant lymphomas have been classified by the WHO into disease categories based not only on histological features, but also on cell surface markers, cytogenetic and clinical features. It is known that chromosome translocation plays an important role in lymphoma development, but it is not entirely clear yet why a given type of chromosome translocation is associated with a specific type of lymphoma. This review deals with molecular mechanisms of B‐cell lymphoma development in association with chromosome translocations. The outcome of chromosome translo‐cations can be categorized into three factors: enhancement of proliferation, inhibition of differentiation and anti‐apoptotic activity. It is well known that chromosome translocation by itself cannot cause cells to become malignant because it is only one of the growth advantages leading to malignancy, while additional genetic and epigenetic alterations are required for cells to become fully malignant. Mucosa‐associated lymphoid tissue (MALT) lymphomas of the stomach are unique in that a majority can be cured by Helicobacter pylori eradication, although 20 to 30% remain resistant. Others as well as we have demonstrated that the presence of the API2‐MALT1 chimeric gene correlates well with resistance to H. pylori eradication treatment. These characteristics have led to the speculation that the classification of MALT lymphoma falls somewhere between tumor and inflammation. Although MALT lymphoma seems to have unique features in comparison with other types of B‐cell lymphomas, it shares common molecular mechanisms with B‐cell lymphoma development.