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

doi:10.1097/MPH.0000000000000183

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 journal › Article › peer-review

2 Scopus citations

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 language	English (US)
Pages (from-to)	e546-e548
Journal	Journal of Pediatric Hematology/Oncology
Volume	36
Issue number	8
DOIs	https://doi.org/10.1097/MPH.0000000000000183
State	Published - Nov 8 2014

Keywords

Acute promyelocytic leukemia
Cytogenetics
Molecular genetics
Therapy induced

ASJC Scopus subject areas

Pediatrics, Perinatology, and Child Health
Hematology
Oncology

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

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).",

keywords = "Acute promyelocytic leukemia, Cytogenetics, Molecular genetics, Therapy induced",

author = "Dang, {Daniel N.} and Morris, {Heather D.} and Feusner, {James H.} and Prasad Koduru and Kathleen Wilson and Timmons, {Charles F.} and Maryellen Cavalier and Luu, {Hung S.}",

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AU - Dang, Daniel N.

AU - Morris, Heather D.

AU - Feusner, James H.

AU - Koduru, Prasad

AU - Wilson, Kathleen

AU - Timmons, Charles F.

AU - Cavalier, Maryellen

AU - Luu, Hung S.

PY - 2014/11/8

Y1 - 2014/11/8

N2 - 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).

AB - 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).

KW - Acute promyelocytic leukemia

KW - Cytogenetics

KW - Molecular genetics

KW - Therapy induced

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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

Abstract

Keywords

ASJC Scopus subject areas

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