The majority of patients with B lymphocyte neoplasms develop a progressive hypoproliferative anemia as the disease progresses. One hypothesis suggests that this anemia is due to abnormal cellular interactions of erythroid stem cells (ESC) with immune lymphocytes. To test this hypothesis, in vitro coculture and cell depletion experiments are proposed to study the growth of ESC in patients with chronic lymphocytic leukemia, multiple myeloma, and non-Hodgkins lymphoma. ESC numbers from blood and marrow of patients with B cell malignancies will be quantified and compared to normal and anemic controls. ESC growth will be correlated with changes in T cell subset ratios in patients with early or advanced disease. T cell subsets will be defined by monoclonal antibodies or differential Fc receptor binding. In some experiments T cells, T cell subsets, B cells, natural killer cells (NK), or monocytes from patients who will be isolated and mixed with autologous or allogeneic marrow or blood ESC enriched fractions in a methylcellulose erythroid culture system. In other experiments the specific lymphocyte subpopulations will be removed prior to culture of ESC. After 7 to 14 days, erythroid colonies will be scored. Isolation, removal, or identification of specific lymphocyte subpopulations will be accomplished by standard immunologic techniques employing sheep erythrocyte rosetting, antibody lysis, immune adherence, and cell affinity chromotography. Similar studies will be carried out in normals for comparison. By understanding the mechanism for the development of the hypoproliferative anemia in B cell neoplasms, rational therapies can be devised to correct the problem. Reduction or elimination of the anemia assocated with some B cell neoplasms will reduce mobidity, delay need for treatment, and improve survival.