Literature DB >> 24942021

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

Daniel N Dang1, Heather D Morris, James H Feusner, Prasad Koduru, Kathleen Wilson, Charles F Timmons, MaryEllen Cavalier, Hung S Luu.   

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 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).

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Year:  2014        PMID: 24942021     DOI: 10.1097/MPH.0000000000000183

Source DB:  PubMed          Journal:  J Pediatr Hematol Oncol        ISSN: 1077-4114            Impact factor:   1.289


  1 in total

1.  Induction of AML Preleukemic Fusion Genes in HSPCs and DNA Damage Response in Preleukemic Fusion Gene Positive Samples.

Authors:  Pavol Kosik; Matus Durdik; Milan Skorvaga; Daniela Klimova; Dominika Kochanova; Zlatica Cerna; Miroslav Kubes; Marek Holop; Igor Belyaev
Journal:  Antioxidants (Basel)       Date:  2021-03-18
  1 in total

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