A five-year-old girl, initially diagnosed as having acute lymphoblastic leukemia (ALL; FAB-L1) relapsed with ALL 4 months after completion of chemotherapy (BFM 83). The initial ALL presentation and subsequent ALL relapse were analyzed using conventional morphology, cytochemistry, cytogenetics and immunophenotyping. The results were consistent with a diagnosis of B-lymphocyte precursor ALL. Bone marrow leukemic cells revealed a 46, XX karyotype at diagnosis and a 46, XX, del(7) (q22; qter) when the girl first relapsed. The case was managed with a BFM REZ-ALL 90 protocol. Upon completion of the first cycle of the protocol, severe myelosuppression developed. This was treated with GM-CSF. Three days later, however, GM-CSF was stopped because the WBC reached 1.1 x 10(9) per liter with 60% of blasts in peripheral blood. Laboratory characteristics were typical of AML. Cytogenetic analysis revealed 46, XX, del(7) (q22; qter) karyotype as before. The bcr-abl fusion gene was not detected. Myeloid blasts were placed in a culture and maintained at 37 degrees C and 7.5% CO2 for two weeks. During this period, formation of hemopoietic colonies was observed and subsequently analyzed using histology and electron microscopy. This showed that the colonies consisted of differentiating erythroid, megakaryocytic and myeloid cells. Further, the chemosensitivity of leukemic cells was examined in both "lymphoid" and "myeloid" relapse instances. While the "lymphoid" phenotype was characterized by good sensitivity to corticosteroids, a typical feature of the "myeloid" phenotype was a high resistance to corticosteroids with marginally increased sensitivity to ARA-C.