Phenylhydrazine stimulates lymphopoiesis and accelerates Abelson murine leukemia virus-induced pre-B cell lymphomas.

Infection of bone marrow or fetal liver cells with Abelson murine leukemia virus (A-MuLV) results in the transformation of pre-B cells and the development of erythroid colonies, indicating that the abl oncogene can affect the growth characteristics of immature cells in both the B cell and erythroid lineages. By comparison, infection of mice with A-MuLV results primarily in the development of pre-B cell lymphomas. To determine whether A-MuLV could induce erythroid disease in vivo, NFS/N mice were pretreated with phenylhydrazine (PHZ) to stimulate erythropoiesis and increase the frequency of potential target cells for A-MuLV. No erythroleukemias developed in mice treated with PHZ. Instead, the latency for pre-B cell lymphomas was reduced by half. This acceleration of disease could be attributed to a marked increase in pre-B cells as targets for transformation by A-MuLV in the bone marrows but not the spleens of treated mice. Increases in the frequencies of T cells in bone marrow and spleen also followed treatment with PHZ. These results show that although PHZ-induced anemia stimulates the production of T and B cells as well as erythroid progenitors, PHZ-treated mice do not develop erythroleukemia or T cell lymphomas. It was also found that the genetically determined resistance of adult C57BL/6 mice to lymphoma induction by A-MuLV could not be overcome by pretreatment with PHZ even though the frequency of pre-B cells in bone marrow was greatly increased by this treatment.