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Treatment‐related acute myelomonocytic leukemia with t(11;19) in a child following chemotherapy for hepatoblastoma

To the Editor: Treatment-related myelodysplastic syndrome/ acute myeloid leukemia (t-MDS/t-AML) is the most serious complication following the treatment of childhood cancer [1]. We describe a child developing AML following chemotherapy for hepatoblastoma as a primary cancer. A healthy Japanese male was born at 40 weeks and 3 days of gestation after uncomplicated pregnancy and had no congenital or hereditary disorders. At 3 months of age, the abdominal computedtomography revealed a large mass occupying the left lobe of the liver. The a-fetoprotein level in his peripheral blood was 159,000 ng/ml, indicating hepatoblastoma. He received CITA therapy (cisplatin and pirarubicin) [2] every 3–4 weeks followed by intrahepatic arterial injection of carboplatin and pirarubicin. Complete tumor resection was done at 9 months of age. The treatment was discontinued at 10 months of age. At this time, the afetoprotein level decreased to 6.6 ng/ml and his peripheral blood fully recovered from chemotherapy. The cumulative doses of drugs were cisplatin 287 mg/m, pirarubicin 245 mg/m, and carboplatin 158 mg/m. He did not receive irradiation. At 17 months of age, his peripheral blood showed WBC 53,960/ml (blast 49.4%), hemoglobin 8.6 g/dl, and platelet 63,000/ml. Immature myeloblasts accounted for 61.0% of nucleated cells in bone marrow, and they were positive for myeloperoxidase, a-naphthyl butyrate, naphthol AS-D chloroacetate, CD 11c, CD13, CD33, and HLA-DR. Cytogenetic analysis revealed a 46, XY, t(11;19)(q23;p13.1) karyotype. These findings indicated the diagnosis of AML, FAB M4.He received combination chemotherapy and achieved complete remission, followed by an allogeneic peripheral blood stem cell transplantation (SCT) from his HLA 2-locus mismatched mother. Six months after SCT, however, AML relapsed and he died of refractory leukemia at 20 months of age. Topoisomerase II inhibitor-related t-MDS/t-AML shows characteristics such as a short latency (1–4 years), FAB M4 or M5 phenotype and cytogenetic abnormalities of 11q23 translocation [1,3]. Out patient received pirarubicin, a topoisomerase II inhibitor, at a total dose of 245 mg/m for hepatoblastoma and developed AMLM4with t(11:19)(q23;p13.1) after a short latency (7 months). A cumulative anthracycline dosemore than 170mg/m significantly increases the risk of t-MDS/t-AML in children with a solid tumor [4]. In Japan, nine cases have been reported to develop leukemia following hepatoblastoma (Supplemental Table I) [5]. All cases except onewere treated with CITA therapy and developed leukemia after a short latency (7–32 months). Eight cases received>170 mg/ m of anthracyclines and five had 11q23 translocation, suggesting topoisomerase II inhibitors to be a causative agent. There has been no report describing Caucasian with t-MDS/t-AML following hepatoblastoma. It is unclear whether the incidence of t-MDS/tAML in children with hepatoblastoma is different between Caucasian and Japanese backgrounds. Hepatoblastoma accounts for 0.9–1.4% of all pediatric cancers in western countries [6,7] and 2.3% in Japan [8]. This difference might affect the incidence of t-MDS/t-AML. Differences in types and doses of chemotherapeutic agents might also influence the incidence [6]. In addition, genetic polymorphisms of metabolizing enzymes for chemotherapeutic drugs are postulated to be involved in the development of t-MDS/tAML [9]. Different frequencies of these polymorphisms have been reported between Caucasian and Japanese [10].