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Detection of myeloperoxidase gene expression by in situ hybridization in a case of granulocytic sarcoma associated with AML-M0

Leukemia volume 15, pages 1797–1799 (2001)Cite this article

Granulocytic sarcomas are uncommon extramedullary tumors composed of myelogenous leukemic cells. They are associated with chronic myelogenous leukemia (CML), myelodysplastic syndrome (MDS), and acute myeloid leukemia (AML).1,2 Although patients occasionally develop localized granulocytic sarcomas, generalized nodal involvement of non-lymphoid leukemia is rare. AML-M0 represents a FAB subtype of acute myeloid leukemia with minimal differentiation in which the blasts show less specific morphological features, with some similarities to lymphoblasts. Granulocytic sarcoma, especially when minimally differentiated, may be difficult to differentiate from non-Hodgkin's lymphomas because they often lack the characteristic myeloid features such as those being determined by chloroacetate esterase, lysozyme, or CD68 antigen tissue section staining. We report here for the first time a case study of a patient with AML-M0 presenting with generalized lymphadenopathy due to granulocytic sarcoma. In situ hybridization (ISH) was used to detect myeloperoxidase (MPO) gene expression as an indicator of myeloid lineage.

A 52-year-old woman presented with right multiple cervical lymphadenopathy on December 1996. A lymph node biopsy was performed, and the tissue was processed for routine histopathological examination only. The features of the lymph node included diffuse infiltrate of medium- or large-sized cells, which were present at all sites of the probe. Initially, the infiltrate appeared to consist of lymphoid cells. Furthermore, immunohistochemical staining showed that the cells were positive for CD45 and CD43. However, antibodies for specific T cell and B cell antigens were negative. Anti-human T cell leukemia virus-I (HTLV-I) antibody was positive. A diagnosis of adult T cell leukemia/lymphoma (ATLL), or peripheral T cell lymphoma, was made. Peripheral blood counts were normal, and the bone marrow aspirate showed normal cellularity without the presence of malignant cells. The patient received six cycles of chemotherapy with CHOP-E (cyclophosphamide 750 mg/m2, doxorubicin 50 mg/m2, vincristine 1.4 mg/m2 all on day 1, etoposide 100 mg/m2 on days 1–3, oral prednisolone 60 mg/m2 on days 1–5) without successful results. We therefore recommended radiation therapy (total 40 Gy) in February 1997. The size of the cervical lymph nodes decreased significantly after radiation therapy. However, the lymph nodal swelling recurred 5 months later. The patient was then admitted to the hospital, and chemotherapy with CHOP-E was performed again. Physical examination showed widespread lymphadenopathy in bilateral cervical, axillary and inguinal regions. Laboratory data showed a white blood cell (WBC) count of 0.5 × 109/l in 55.5% of the small undifferentiated blasts, with a high nucleus-to-cytoplasm ratio; a hemoglobin (Hb) level of 8.1 g/dl; a platelet count (PLT) of 35 × 109/l; lactic dehydrogenase (LDH) was 160 IU/l; and the serum level of the soluble interleukin-2 receptor (sIL-2R) was 848 U/ml (normal 220–530 U/ml). Bone marrow aspiration demonstrated a normocellular marrow with 84% of the small undifferentiated blasts, with a high nucleus-to-cytoplasm ratio. Auer rod and azurophilic granules were not found. Histochemical stains of blasts for myeloperoxidase, Sudan black B, periodic acid-schiff, non-specific esterase, and double esterase were all negative. Cell markers showed the presence of CD13 (55.6%), CD33 (99.1%), CD34 (85.3%), CD7 (99.7%), and HLA-DR (60.9%). CD3, CD4, CD5, CD16, CD19, CD20, and CD56 tests were negative. Karyotypic analysis showed 46XX, t(7;14) (p15;q32), add(18) (p11.2) [10/20], 46XX, t(7;14) (p15;q32) [1/20], 44XX, add(3) (q2.1), −5, t(7;14) (p15;q32), −9, −13, −16, add(17) (p11.2), add(18) (p11.2), +2mar [1/20]. A rearranged band in the T cell antigen receptor (TCR)-Cβ1, TCR-Cβ2, TCR-Jβ1, TCR-Jβ2, TCR-Jγ, TCR-Jδ chains, and immunoglobulin-heavy and -light chains was not detected by Southern blot analysis. A diagnosis of AML-M0 was made according to the FAB guidelines proposed by Bennett et al.3 Moreover, an inguinal lymph node biopsy was performed. The patient underwent chemotherapy with CAG (cytarabine 10 mg/m2 on days 1–14, aclarubicin 14 mg/m2 on days 1–4, and G-CSF 200 μg/m2 on days 1–14). Blasts in the bone marrow aspiration and peripheral blood gradually decreased, and pancytopenia progressed in the patient's peripheral blood. However, swelling of the cervical, inguinal, and para-aortic lymph nodes has progressed 9 months after diagnosis. The patient ultimately died of cerebral and pulmonary bleeding.

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Acknowledgements

We wish to thank Mr Yoichi Tani and Mr Koichiro Kitagawa (Dako Lab, Dako Japan) for their valuable assistance with the in situ hybridization for MPO.

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  1. Third Department of Internal Medicine, Kinki University School of Medicine, Osaka, Japan

    H Miyazato, H Sono, Y Naiki, J Miyatake, Y Nozaki, T Yamaguchi, M Matsuda, Y Tatsumi, Y Maeda & A Kanamaru

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Miyazato, H., Sono, H., Naiki, Y. et al. Detection of myeloperoxidase gene expression by in situ hybridization in a case of granulocytic sarcoma associated with AML-M0. Leukemia 15, 1797–1799 (2001). https://doi.org/10.1038/sj.leu.2402270

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