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Therapy-induced Secondary Acute Myeloid Leukemia With t(11;19)(q23;p13.1) in a Pediatric Patient With Relapsed Acute Promyelocytic Leukemia

Dang, Daniel N. MD*; Morris, Heather D. DO*; Feusner, James H. MD; Koduru, Prasad PhD*; Wilson, Kathleen MD*; Timmons, Charles F. MD, PhD*; Cavalier, MaryEllen MD; Luu, Hung S. PharmD, MD*

Journal of Pediatric Hematology/Oncology: November 2014 - Volume 36 - Issue 8 - p e546–e548
doi: 10.1097/MPH.0000000000000183
Online Articles: Clinical and Laboratory Observations

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:

Received November 13, 2013

Accepted April 30, 2014

© 2014 by Lippincott Williams & Wilkins.