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Amifostine is a phosphorylated aminothiol that not only protects hematopoietic progenitor cells from chemotherapy and radiotherapy, but also stimulates normal hematopoiesis. The effect of amifostine on the in vitro growth of hematopoietic progenitors derived from B-cell chronic lymphocytic leukemia(B-CLL) was investigated. The colony-forming units (CFU)-granulocyte macrophage (CFU-GM), the burst-forming units-erythroid (BFU-E) and the CFU-granulocyte erythroid macrophage megakaryocytes (CFU-GEMM) increased 38, 20 and 100%, respectively, after the incubation with amifostine. There was no statistical difference in the in vitro progenitor growth of patients grouped according to their disease stage, bone marrow lymphocytic infiltration or therapy. Our data indicate that apart from cytoprotection the parallel use of amifostine and chemotherapy in patients with B-CLL could enhance bone marrow recovery.

We assayed granulocyte‐macrophage committed progenitor cells (CFU‐GM) in the peripheral blood of 34 patients with chronic lymphocytic leukemia (CLL) and 12 normal individuals. The patients were divided into separate groups on the basis of previous therapy (i.e. analysis performed at diagnosis, during and after chemotherapy) and clinical features of the disease (i.e. disease stage, pattern of bone marrow infiltration, peripheral blood lymphocytosis). The mean CFU‐GM colony count of the patients was 30 times higher than that of the controls (206.4 ± 197.8 (SD) CFU‐GM per 5 times 105 cells plated versus 6.5 ± 3.6). There was no statistical difference in the numbers of circulating CFU‐GM between the patients studied at diagnosis (257 ± 215.4 CFU‐GM/5 times 105 cells) and those studied during (117.6 ± 169.2 CFU‐GM/5 times 105 cells) or after chemotherapy (207.5 ± 105.9 CFU‐GM/5 times 105 cells), although a trend towards a higher recovery of myeloid progenitors was observed as a function of time elapsing from the last treatment. In addition, we found no significant difference in the in vitro CFU‐GM growth of patients grouped according to their disease stage, pattern of bone marrow infiltration and degree of peripheral blood lymphocytosis. In conclusion, our data indicate that intensification with peripheral blood stem cell support may be feasible in CLL, since progenitor cells of myeloid‐monocytic series are markedly increased in the peripheral blood of these patients. Moreover, it is possible to extend this kind of therapy to patients who have undergone previous extensive chemotherapy and who might have persisting bone marrow infiltration.

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