Proliferation of B cell precursors in bone marrow of pristane-conditioned and malaria-infected mice: implications for B cell oncogenesis.

Two widely different agents implicated in the etiology of neoplasias of the B cell lineage, pristane and malaria, have both been found to produce a prolonged increase in the level of proliferative activity and cell production by early B lymphocyte precursor cells in mouse bone marrow. This apparently leads to an elevated level of cell loss, suggesting the production of many aberrant early cells. The mechanism and significance of this effect remain to be determined. However, the present findings focus attention on the early stages of B cell genesis in the bone marrow as possible target cells for the initiation of genetic events leading to neoplasia. Together with previous work, the results suggest that pathologically elevated levels of macrophage activation may play a role in predisposing to various B cell neoplasias.