Therapy-induced secondary acute myeloid leukemia with t(11;19)(q23;p13.1) in a pediatric patient with relapsed acute promyelocytic leukemia

Daniel N. Dang, Heather D. Morris, James H. Feusner, Prasad Koduru, Kathleen Wilson, Charles F. Timmons, Maryellen Cavalier, Hung S. Luu

Research output: Contribution to journalArticle

Abstract

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 alltrans 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).

Original languageEnglish (US)
Pages (from-to)e546-e548
JournalJournal of Pediatric Hematology/Oncology
Volume36
Issue number8
DOIs
StatePublished - Nov 8 2014

Keywords

  • Acute promyelocytic leukemia
  • Cytogenetics
  • Molecular genetics
  • Therapy induced

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Hematology
  • Oncology

Fingerprint Dive into the research topics of 'Therapy-induced secondary acute myeloid leukemia with t(11;19)(q23;p13.1) in a pediatric patient with relapsed acute promyelocytic leukemia'. Together they form a unique fingerprint.

  • Cite this