Relapsed acute monocytic leukemia presenting as histiocytic morphology
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IMAGES IN HEMATOLOGY
Relapsed acute monocytic leukemia presenting as histiocytic morphology Bing Liu1 · Ting Li2 Received: 16 February 2020 / Revised: 5 August 2020 / Accepted: 7 September 2020 © Japanese Society of Hematology 2020
Keywords Acute monoblastic leukaemia · Histiocytic morphology · Immunophenotyping · Second-generation sequencing A 10-year-old boy was admitted to hospital for the 8th routine reexamination of the marrow, with a 17-month history of acute monocytic leukemia. At the time of the initial diagnosis, bone marrow (BM) aspirate films were replaced by round-shaped blasts with regular nuclei, agranular and moderately blue cytoplasm, delicate lacy chromatin with multiple variably nucleoli ranging from inconspicuous to prominent, accounting for 83.2% of the marrow cellularity (Fig. 1a, b). These leukemic cells had no obviously histiocytic features. Myeloperoxidase staining was negative. Nearly all the leukemic cells were positive for alpha naphthyl acetate esterase (ANAE), the activities varying from moderate to strong, and the ANAE activity of the cells was completely inhibited by the sodium fluoride (NaF). Immunophenotyping showed the abnormal cells were positive for HLA-DR, CD38, CD13, CD123, CD33, CD56, CD11c, CD117, CD15, CD11b and CD64, but negative for CD34, CD2, CD19, CD7, CD10, CD20, CD3, CD4, CD5, CD16, CD36, CD14, CD25, CD303, cCD79a, cCD3 and cMPO. Cytogenetic analysis identified a t(11;19)(q23;p13.3). Reverse transcriptase polymerase chain reaction (RT-PCR) detected the KMT2A-MLLT1 rearrangement. By the way, breakpoints within subband 19p13.3 are found in both ALL and AML with the translocation t(11;19)(q23;p13.3) leading to the fusion of KMT2A (previously called MLL and HRX) with MLLT1 (also known as ENL and LTG19) generating * Ting Li [email protected] 1
Department of Clinical Laboratory, Henan Cancer Hospital, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou 450008, Henan Province, China
Department of Flow Cytometry, Beijing Lu DaoPei Hospital, No. 22 Tongji South Road, Yizhuang Economic‑Technological Development Area, Beijing 100076, China
2
an KMT2A-MLLT1 fusion gene. Hence, a diagnosis of acute monoblastic leukaemia was made. While this time, laboratory findings showed white blood cell count 67.35 × 109/L, the red blood cell count 2.36 × 1012/L, hemoglobin of 78 g/L and platelet 38 × 109/L. BM smear revealed 71% monoblasts with 20.4% promonocytes, resembling histiocytes with irregular nuclei, showing a high nucleocytoplasmic ratio with plenty of cytoplasm, containing oval nuclei with finely reticulated nuclear chromatin with regular outlines and between one and three prominent nucleoli (Fig. 1c, d). The BM aspirate films were negative for CD1a and S100 by immunostaining. The leukemic blasts had almost the same myeloperoxidase staining, the ANAE activity, immunophenotype, t(11;19)(q23;p13.3) and KMT2A-MLLT1 rearrangement as at initial diagnosis. Next Generation Sequencing detected KMT2C gene and NRAS mutations. The point mutation of KMT2C was exon38,
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