Case Report

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Korean J Hematol 2012; 47(3):

Published online September 25, 2012

https://doi.org/10.5045/kjh.2012.47.3.225

© The Korean Society of Hematology

A case of therapy-related acute myeloid leukemia with inv(16)(p13.1q22) after single low-dose iodine-131 treatment for thyroid cancer

Ji Hun Jeong1, Jeong Yeal Ahn1*, Soon Ho Park1, Mi Jung Park1, Kyung Hee Kim1, and Jun Shik Hong2

1Department of Laboratory Medicine, Gachon University Gil Medical Center, Incheon, Korea.

2Department of Internal Medicine, Gachon University Gil Medical Center, Incheon, Korea.

Correspondence to : Correspondence to Jeong Yeal Ahn, M.D. Department of Laboratory Medicine, Gachon University Gil Medical Center, 1198, Guwol-dong, Namdong-gu, Incheon 405-706, Korea. Tel: +82-32-460-3863, Fax: +82-32-460-3415, jyahn@gilhospital.com

Received: December 30, 2011; Revised: March 27, 2012; Accepted: August 3, 2012

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Radioiodine is regularly used in the treatment of thyroid cancer to eliminate residual malignant tissue after thyroidectomy and to treat metastasis. Because of the low dose of radioiodine used to treat thyroid cancer patients, leukemia is an uncommon complication of exposure to radioiodine. Here, we present a patient who developed therapy-related acute myeloid leukemia with inv(16)(p13.1q22);CBFβ-MYH11, eosinophilia, and K-ras mutation and who had been treated with very low-dose radioiodine following total thyroidectomy.

Keywords Radioiodine, Thyroid cancer, Acute myeloid leukemia, CBFβ-MYH11, Eosinophilia, K-ras

Article

Case Report

Korean J Hematol 2012; 47(3): 225-228

Published online September 25, 2012 https://doi.org/10.5045/kjh.2012.47.3.225

Copyright © The Korean Society of Hematology.

A case of therapy-related acute myeloid leukemia with inv(16)(p13.1q22) after single low-dose iodine-131 treatment for thyroid cancer

Ji Hun Jeong1, Jeong Yeal Ahn1*, Soon Ho Park1, Mi Jung Park1, Kyung Hee Kim1, and Jun Shik Hong2

1Department of Laboratory Medicine, Gachon University Gil Medical Center, Incheon, Korea.

2Department of Internal Medicine, Gachon University Gil Medical Center, Incheon, Korea.

Correspondence to:Correspondence to Jeong Yeal Ahn, M.D. Department of Laboratory Medicine, Gachon University Gil Medical Center, 1198, Guwol-dong, Namdong-gu, Incheon 405-706, Korea. Tel: +82-32-460-3863, Fax: +82-32-460-3415, jyahn@gilhospital.com

Received: December 30, 2011; Revised: March 27, 2012; Accepted: August 3, 2012

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Radioiodine is regularly used in the treatment of thyroid cancer to eliminate residual malignant tissue after thyroidectomy and to treat metastasis. Because of the low dose of radioiodine used to treat thyroid cancer patients, leukemia is an uncommon complication of exposure to radioiodine. Here, we present a patient who developed therapy-related acute myeloid leukemia with inv(16)(p13.1q22);CBFβ-MYH11, eosinophilia, and K-ras mutation and who had been treated with very low-dose radioiodine following total thyroidectomy.

Keywords: Radioiodine, Thyroid cancer, Acute myeloid leukemia, CBFβ-MYH11, Eosinophilia, K-ras

Fig 1.

Figure 1.

Morphologic and cytogenetic study. (A) Peripheral blood smear and (B) bone marrow aspirates show myeloblasts, immature monocyte precursors, and abnormal eosinophils. The eosinophil count is markedly increased (53.4%), and some eosinophils have basophilic granules (Wright Giemsa stain ×1,000). (C) Blasts are positive for myeloperoxidase (MPO). (D) The marrow monocytic component is stained by α-naphthyl-butyrate esterase. (E) The karyotype reveals 46,XX,inv (16)(p13.1q22)[20] (GTL banding, ×1,000). (F) FISH using a LSI CBFB Dual Color Break Apart Rearrangement Probe reveals separate red (5' CBFB gene) and green (3' CBFB gene) signals, resulting in distinct hybridization signals on the arm of the inverted chromosome 16, and these signals were expressed in more than 89% of the cells. The normal CBFB allele is seen as one fused red-green (yellow) signal.

Blood Research 2012; 47: 225-228https://doi.org/10.5045/kjh.2012.47.3.225

Fig 2.

Figure 2.

K-ras mutation by pyrosequencing. Pyrogram shows the mutation and mutated clones. The X axis means the base and the Y axis represents the intensity of fluorescent signal. Shaded regions represent K-ras codons 12 and 13. (A) Arrow shows the analytic results of substitutions in the second base of K-ras codon 12. The mutation GGT (Gly) to GAT (Asp) in codon 12 was detected by pyrosequencing. (B) After induction of chemotherapy, the K-ras mutation disappeared.

Blood Research 2012; 47: 225-228https://doi.org/10.5045/kjh.2012.47.3.225
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