Acute myeloid leukemia with T-lymphoid expression and distinct chromosomal abnormalities.

The report by Cuneo et all on adult acute myeloid leukemia (AML) expressing lymphoid markers illustrates an interesting clinicopathologic problem that we have recently encountered. A 20-year-old man presented with bilateral tonsillar enlargement and lymphadenopathy in the cervical, axillary, and inguinal regions. Full blood count was: hemoglobin 88 g/L, white blood cell count 57 x 109/L, platelets 69 x 109/L. The bone marrow was hypercellular with 93% blasts, some with coarse granules but no Auer rods. Sudan Black was faintly positive in 3% of the blasts. A working diagnosis of AML (French-American-British [FABI-M1) was made and the patient was randomized in the DAT 3 + 10 arm of the Medical Research Council (MRC) AMLlO trial protocol. Subsequently immunophenotyping from two different laboratories gave the results summarized (Table 1). These results were discrepant for the following reasons. First, cytoplasmic CD3 reactivity was negative in one laboratory. Secondly, Tdt reactivity was ambiguous from one laboratory but definitive from the other. Lastly, TCR 6y gene rearrangement was positive in one laboratory and not tested in the other. Thus, both laboratories showed coexpression of myeloid and T-lymphoid markers but emphasis was subtly different, one tending toward a lymphoid and the other toward a myeloid interpretation. Cytogenetic analysis of the marrow leukemic cells showed hyperploidy in