PMID: 9631585Jun 19, 1998Paper

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
K TakedaK Ariyoshi

Abstract

A 59-year-old female suffering from malignant lymphoma developed therapy-related acute myeloblastic leukemia (t-AML) after chemotherapy consisting of treatment with DNA-topoisomerase II inhibitors, etoposide and mitoxantrone, and an alkylating agent, cyclophosphamide. The cumulative dose of etoposide administration was 5500 mg; 1500 mg given intravenously and 4000 mg orally. One year later, she suddenly developed AML of FAB M2. Cytogenetic analysis of bone marrow cells revealed deletion of 7q and a rare translocation, t(16;21)(q24;q22). Southern blot analysis of bone marrow cells did not detect rearrangement of the AML1 gene, however, fluorescence in situ hybridization (FISH) analysis of bone 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 breakpoint cluster region for t(8;21). The patient was treated with chemotherapy and entered complete remission.

Citations

Nov 9, 2010·Leukemia & Lymphoma·Anastasia AthanasiadouAchilles Anagnostopoulos
Feb 10, 2007·Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology·Cameron K TebbiCindy L Schwartz
Feb 21, 2008·Acta Haematologica·Christie L Boils, Anwar N Mohamed

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