Malignant B Cells and Antigenic Receptor: Necessity or Habit?

Abstract

B-cell malignancies account for the majority of lymphoid tissue neoplasia. Similar to normal B cells, malignant B cells in most Hodgkin's and non-Hodgkin's types of lymphomas express B-cell receptor (BCR) on their membrane. Since neoplastic B cells retain the capacity to respond to microenvironmental signals, and in many respects still behave as normal B cells, it does not seem bizarre that the BCR, which dominates the biology of normal B cells, can remain equally important for some malignant B cells. Indirect evidence suggests that retained BCR expression, and in certain cases coupled with stimulation by antigen (Ag), may be necessary for the viability of some B-cell tumors. The aim of this review is to consider the evidence regarding the role of the BCR in tumorigenesis of B-cell lymphomas, and discuss different approaches used in evaluating this role in the persistence and progression of these malignancies. The diversity in B-cell lymphomas prevents easy classification of these cancers based on their dependence on BCR expression. It seems likely that some malignant B cells need BCR expression, or additionally, stimulation by Ag in order to survive. However, through accumulation of additional genetic changes, the original tumor can give rise to a clone that no longer requires signals from the BCR to survive. Thus, most B-cell lymphomas may initially retain dependence on BCR expression that governs normal B-cell physiology and may lose it only at later stages of tumor progression, through the accumulation of additional transforming events.

• B Cell
• Malignancy
• B-cell Receptor
• Clonal Evolution