A CASE OF THERAPY-RELATED ACUTE MYELOBLASTIC-LEUKEMIA WITH T(16-21)(Q24-Q22) AFTER CHEMOTHERAPY WITH DNA-TOPOISOMERASE-II INHIBITORS, ETOPOSIDE AND MITOXANTRONE, AND THE ALKYLATING AGENT, CYCLOPHOSPHAMIDE

A 59-year-oId female suffering from malignant lymphoma developed thera py-related acute myeloblastic leukemia (t-AML) after chemotherapy cons isting of treatment with DNA-topoisomerase II inhibitors, etoposide an d mitoxantrone, and an alkylating agent, cyclophosphamide. The cumulat ive dose of etoposide administration was 5500 mg; 1500 mg given intrav enously and 4000 mg orally. One year later, she suddenly developed AML of FAB M2. Cytogenetic analysis of bone marrow cells revealed deletio n of 7q and a rare translocation, t(16;21)(q24;q22). Southern blot ana lysis of bone marrow cells did not detect rearrangement of the AML1 ge ne, however, fluorescence in situ hybridization (FISH) analysis of bon e marrow cells at interphase and metaphase revealed a translocational splitting between chromosome 21 involving AML1 gene and chromosome 16. These results suggest that the breakpoint is not located in the break point cluster region for t(8;21). The patient was treated with chemoth erapy and entered complete remission. (C) 1998 Elsevier Science Irelan d Ltd. All rights reserved.