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
K. Takeda et al., 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, International journal of hematology, 67(2), 1998, pp. 179-186
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.