Treatment-related Myelodysplastic Syndrome in a Child With Acute Myeloid Leukemia and TPMT Heterozygosity

Lars M Stensman; Eigil Kjeldsen; Jacob Nersting; K. Schmiegelow; Henrik Hasle

doi:10.1097/MPH.0000000000000211

Treatment-related Myelodysplastic Syndrome in a Child With Acute Myeloid Leukemia and TPMT Heterozygosity

Lars M Stensman, Eigil Kjeldsen, Jacob Nersting, K. Schmiegelow, Henrik Hasle

Institut for Klinisk Medicin

2 Citationer (Scopus)

Abstract

INTRODUCTION: We describe a patient diagnosed with acute myeloid leukemia (AML) and low activity of thiopurine methyltransferase (TPMT) who developed secondary myelodysplastic syndrome after treatment.

OBSERVATION: A 10-year-old boy presented with AML-M2 with t(8;21)(q22;q22) and genotyping revealing 3*B TPMT heterozygosity. The patient was treated according to the NOPHO-AML 2004 protocol. Two years after the treatment, the patient presented with neutropenia and thrombocytopenia. Bone marrow, including fluorescent in situ hybridization and retrospective aCGH analysis, verified therapy-related myelodysplastic syndrome with ring chromosome 6.

DISCUSSION: The clinical course of this patient raises the possibility that low-activity TPMT genotypes may influence 6TG toxicity in patients with AML and lead to an increased risk of developing secondary malignant neoplasms.

Originalsprog	Engelsk
Tidsskrift	Journal of Pediatric Hematology/Oncology
Vol/bind	37
Udgave nummer	4
Sider (fra-til)	e242–e244
Antal sider	3
ISSN	1077-4114
DOI	https://doi.org/10.1097/MPH.0000000000000211
Status	Udgivet - 1 dec. 2015

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10.1097/MPH.0000000000000211

Citationsformater

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title = "Treatment-related Myelodysplastic Syndrome in a Child With Acute Myeloid Leukemia and TPMT Heterozygosity",

abstract = "INTRODUCTION: We describe a patient diagnosed with acute myeloid leukemia (AML) and low activity of thiopurine methyltransferase (TPMT) who developed secondary myelodysplastic syndrome after treatment.OBSERVATION: A 10-year-old boy presented with AML-M2 with t(8;21)(q22;q22) and genotyping revealing 3*B TPMT heterozygosity. The patient was treated according to the NOPHO-AML 2004 protocol. Two years after the treatment, the patient presented with neutropenia and thrombocytopenia. Bone marrow, including fluorescent in situ hybridization and retrospective aCGH analysis, verified therapy-related myelodysplastic syndrome with ring chromosome 6.DISCUSSION: The clinical course of this patient raises the possibility that low-activity TPMT genotypes may influence 6TG toxicity in patients with AML and lead to an increased risk of developing secondary malignant neoplasms.",

author = "Stensman, {Lars M} and Eigil Kjeldsen and Jacob Nersting and K. Schmiegelow and Henrik Hasle",

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TY - JOUR

T1 - Treatment-related Myelodysplastic Syndrome in a Child With Acute Myeloid Leukemia and TPMT Heterozygosity

AU - Stensman, Lars M

AU - Kjeldsen, Eigil

AU - Nersting, Jacob

AU - Schmiegelow, K.

AU - Hasle, Henrik

PY - 2015/12/1

Y1 - 2015/12/1

N2 - INTRODUCTION: We describe a patient diagnosed with acute myeloid leukemia (AML) and low activity of thiopurine methyltransferase (TPMT) who developed secondary myelodysplastic syndrome after treatment.OBSERVATION: A 10-year-old boy presented with AML-M2 with t(8;21)(q22;q22) and genotyping revealing 3*B TPMT heterozygosity. The patient was treated according to the NOPHO-AML 2004 protocol. Two years after the treatment, the patient presented with neutropenia and thrombocytopenia. Bone marrow, including fluorescent in situ hybridization and retrospective aCGH analysis, verified therapy-related myelodysplastic syndrome with ring chromosome 6.DISCUSSION: The clinical course of this patient raises the possibility that low-activity TPMT genotypes may influence 6TG toxicity in patients with AML and lead to an increased risk of developing secondary malignant neoplasms.

AB - INTRODUCTION: We describe a patient diagnosed with acute myeloid leukemia (AML) and low activity of thiopurine methyltransferase (TPMT) who developed secondary myelodysplastic syndrome after treatment.OBSERVATION: A 10-year-old boy presented with AML-M2 with t(8;21)(q22;q22) and genotyping revealing 3*B TPMT heterozygosity. The patient was treated according to the NOPHO-AML 2004 protocol. Two years after the treatment, the patient presented with neutropenia and thrombocytopenia. Bone marrow, including fluorescent in situ hybridization and retrospective aCGH analysis, verified therapy-related myelodysplastic syndrome with ring chromosome 6.DISCUSSION: The clinical course of this patient raises the possibility that low-activity TPMT genotypes may influence 6TG toxicity in patients with AML and lead to an increased risk of developing secondary malignant neoplasms.

U2 - 10.1097/MPH.0000000000000211

DO - 10.1097/MPH.0000000000000211

M3 - Journal article

C2 - 25000470

SN - 1077-4114

VL - 37

SP - e242–e244

JO - Journal of Pediatric Hematology/Oncology

JF - Journal of Pediatric Hematology/Oncology

IS - 4

ER -

Treatment-related Myelodysplastic Syndrome in a Child With Acute Myeloid Leukemia and TPMT Heterozygosity

Abstract

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