LAUSR

A 27-year-old female with a history of acute myeloid leukaemia (AML) with t(8;21)(q22;q22.1); RUNX1-RUNX1T1, in remission, presented for routine bone marrow (BM) followup. Her full blood count was normal. The BM aspirate film, however, showed a few scattered myeloblasts (2% of total cells) with either large salmon-coloured granules/pseudoCh ediak–Higashi granules (top left, orange arrow; Wright– Giemsa stain, 9100 objective) or Auer rods intermingled with salmon-coloured granules (bottom left, green arrow). Interestingly, some mature dysplastic neutrophils with pseudo-Pelger–Hu€et nuclei also had multiple large salmoncoloured cytoplasmic granules (right, orange arrow, 9100). Concurrent flow cytometric immunophenotyping revealed a small population of neoplastic myeloblasts (0.65% of total cells) with a distinctly aberrant immunophenotype: loss of myeloid marker (CD13 ), maturation asynchrony (CD15/ CD34) and expression of lymphoid markers (CD19/ CD56). Fluorescence in situ hybridisation confirmed the persistence of RUNX1-RUNX1T1 fusion in 6% of interphase cells. In summary, large cytoplasmic salmon-coloured granules and Auer rods in myeloblasts and aberrant expression of CD19 and CD56 by myeloblasts are characteristic findings in AML with RUNX1-RUNX1T1. The pseudo-Ch ediak–Higashi granules in mature neutrophils are, however, an uncommon finding. Recognition of these features is important in establishing a diagnosis of residual AML.