Acute myeloid leukemia is classified based upon recurrent cytogenetic abnormalities. The t(15;17)(q24.1;q21.1) abnormality is found in 5% to 8% of de novo acute myeloid leukemia and is diagnostic of acute promyelocytic leukemia (APL). The translocation results in fusion of the retinoic acid receptor-α (RARA) gene at 17q21.1 and the promyelocytic leukemia (PML) gene at 15q24.1. Standard APL therapy is a combination of all-trans retinoic acid and anthracycline-based chemotherapy. Anthracycline treatment is associated with secondary clonal chromosomal aberrations that can lead to therapy-related secondary myeloid neoplasms. We present a pediatric case of relapsed APL coexistent with treatment-associated secondary myeloid neoplasm with t(11;19)(q23;p13.1).
*Department of Pathology, Parkland Health and Hospital System, Children’s Medical Center
‡Department of Pediatrics, Division of Hematology-Oncology, UT Southwestern Medical Center, Dallas, TX
†Department of Pediatrics, Division of Hematology/Oncology, Children’s Hospital & Research Center Oakland, Oakland, CA
The authors declare no conflict of interest.
Reprints: Hung S. Luu, PharmD, MD, Department of Pathology, Parkland Health and Hospital System, Children’s Medical Center, UT Southwestern Medical Center, 1935 Medical District Drive, Dallas, TX 75235 (e-mail: firstname.lastname@example.org).
Received November 13, 2013
Accepted April 30, 2014