Relapsed acute monocytic leukemia presenting as histiocytic morphology

Excerpt

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 an KMT2A-MLLT1 fusion gene. Hence, a diagnosis of acute monoblastic leukaemia was made.

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