Mechanisms of B-cell lymphoma pathogenesis

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Abstract
A hallmark of many types of B-cell lymphoma is reciprocal chromosomal translocations involving one of the immunoglobulin loci and a proto-oncogene. As a consequence of such translocations, the oncogene comes under the control of an active immunoglobulin locus, causing deregulated, constitutive expression of the translocated gene. Normal B cells depend on B-cell receptor (BCR) expression for survival. The selection for expression of a BCR also seems to operate in most malignant B cells. Although there is strong evidence that most B-cell lymphomas depend on BCR expression, there are a few exceptions — namely classical Hodgkin's lymphoma, primary mediastinal B-cell lymphoma, some post-transplant lymphomas, and the rare primary effusion lymphomas. In several lymphomas, there is a strong indication that the lymphoma cells recognize an antigen and that stimulation by antigen binding contributes to the survival and proliferation of lymphoma cells. In many lymphomas, such as follicular lymphoma, mucosa-associated lymphoid tissue lymphomas and classical Hodgkin's lymphoma, the tumour microenvironment seems to be important for the survival and/or proliferation of the lymphoma cells. The recognition that the survival and/or proliferation of many B-cell lymphomas depends on their interaction with other cells in the microenvironment, as well as on expression of the B-cell receptor and, sometimes, antigen activation, might lead to novel treatment options for B-cell lymphomas.