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Therapy-related Acute Myeloid Leukemia Following Treatment for Burkitt’s Lymphoma

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229

Letters to the Editor

www.cmj.ac.kr

https://doi.org/10.4068/cmj.2017.53.3.229

Chonnam Medical Journal, 2017 Chonnam Med J 2017;53:229-230

Corresponding Author:

Seung-Shin Lee

Department of Hematology-Oncology, Chonnam National University Hwasun Hospital, 322 Seoyang-ro, Hwasun 58128, Korea

Tel: +82-61-379-7636, Fax: +82-61-379-7628, E-mail: pepupa80@gmail.com

Article History:

Received July 15, 2017 Revised July 30, 2017 Accepted August 2, 2017 FIG. 1. Microscopic images show a monotonous infiltrate of me- dium-sized lymphoid cells with round, non-cleaved nuclei (hematoxylin and eosin stain, ×200) (A) and a strong positivity (>99% of all malignant cells) in immunohistochemical stain for the cell proliferation marker Ki-67 (B). Bone marrow aspirate shows increased numbers of blasts with some cytoplasmic va- cuoles and azurophilic granules (Wright stain, ×1,000) (C).

Therapy-related Acute Myeloid Leukemia Following Treatment for Burkitt’s Lymphoma

Seung-Shin Lee*

Department of Hematology-Oncology, Chonnam National University Hwasun Hospital, Hwasun, Korea

Therapy-related, acute myeloid leukemia (t-AML) is a rare form of AML and is usually reported in association with chemotherapies that include alkylating agents, epi- podophyllotoxin, as well as radiotherapy. t-AML generally develops years after treatments for the primary malig-

nancy and has a poor prognosis.1,2 The incidence of t-AML is about 0.18% according to the United States popula- tion-based cancer registry study.3 Herein, the first case of t-AML is reported in a patient with Burkitt’s lymphoma (BL) treated with multiple chemotherapeutic agents with-

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230

Therapy-related Acute Myeloid Leukemia Following Treatment for Burkitt’s Lymphoma

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/

by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

out epipodophyllotoxin.

A 55-year-old male patient complaining of submental and nasopharyngeal masses was admitted to our hospital.

The excised mass was positive for the leukocyte common antigens, CD20, CD79a, and Ki-67 (nearly 100%) and the diagnosis of BL was confirmed (Fig. 1A, B). The karyotype of the bone marrow (BM) cells was 46,XY. The patient was treated with eight cycles of the hyper-fractionated CVAD regimen (cyclophosphamide, vincristine, doxorubicin, and dexamethasone), alternated with high-dose methotrexate and cytarabine. A complete response was obtained after two cycles of chemotherapy.

A complete blood count, 20 months after the last cycle, showed pancytopenia (white blood cells 6.22×109/L, hemo- globin 6.8 g/dL and platelet 24×109/L). The blood count at the time of diagnosis of BL was within normal ranges (white blood cells 7.93×109/L, hemoglobin 13.5 g/dL and platelet 261×109/L). A BM examination (Fig. 1C) revealed that about 30% blast cells (positive for CD13, CD33, CD34, HLA-DR, and myeloperoxidase, but negative for lymphoid markers). A chromosomal analysis of the BM cells showed 47,XY,+3,del(7)(q31.2q34),t(16;21)(q24;q22), and the pa- tient was diagnosed with t-AML. Standard induction che- motherapy was administered, and one cycle of consolida- tion chemotherapy was added after complete remission.

Finally, the patient underwent allogeneic stem cell trans- plantation and has been doing well for more than 2 years without recurrence of AML or BL.

t-AML is an important issue for clinicians, as it is thought to be a consequence of a mutation by prior treat- ment that can develop after successful chemotherapies for primary malignancies. t-AML is characterized by a latency of 5-7 years after exposure to alkylating agents or radiation therapy as well as complex karyotype and monosomy of chromosomes 5 and 7.4 Many case series in the early 1990s revealed an association between epipodophyllotoxin and t-AML in children with acute lymphoblastic leukemia. In

these reports, the latent period ranged from 1 to 3 years and cytogenetic abnormalities involving 11q23 were common.1

Pancytopenia developed 20 months after completion of chemotherapy in this case of t-AML, which was first as- sumed to be the consequence of BL recurrence with BM involvement. However, a computed tomography scan and the BM results suggested a diagnosis of t-AML. Although the latency is relatively short, considering the complex kar- yotype, it seems to be associated with an alkylating agent.

The only treatment option given the poor prognosis of t-AML was allogeneic stem cell transplantation.

In conclusion, t-AML can develop within 2 years follow- ing chemotherapy for BL. Allogeneic stem cell trans- plantation is mandatory in eligible patients considering the poor prognosis of t-AML.

CONFLICT OF INTEREST STATEMENT None declared.

REFERENCES

1. Sandler ES, Friedman DJ, Mustafa MM, Winick NJ, Bowman WP, Buchanan GR. Treatment of children with epipodophyllotox- in-induced secondary acute myeloid leukemia. Cancer 1997;79:

1049-54.

2. Winick NJ, McKenna RW, Shuster JJ, Schneider NR, Borowitz MJ, Bowman WP, et al. Secondary acute myeloid leukemia in chil- dren with acute lymphoblastic leukemia treated with etoposide.

J Clin Oncol 1993;11:209-17.

3. Morton LM, Dores GM, Tucker MA, Kim CJ, Onel K, Gilbert ES, et al. Evolving risk of therapy-related acute myeloid leukemia fol- lowing cancer chemotherapy among adults in the United States, 1975-2008. Blood 2013;121:2996-3004.

4. Zeichner SB, Arellano ML. Secondary adult acute myeloid leuke- mia: a review of our evolving understanding of a complex disease process. Curr Treat Options Oncol 2015;16:37.

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