t(3;21)(q26;q22) with AML1 rearrangement in a de novo childhood acute monoblastic leukaemia

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Abstract
T(3;21)(q26;q22) is a recurrent chromosomal abnormality in Philadelphia‐positive chronic myeloid leukaemia in blast crisis and in treatment‐related myelodysplastic syndrome and acute myeloid leukaemia. The molecular consequences of the t(3;21) are presently being unravelled; various transcripts between the AML1 gene in 21q22 and several unrelated genes, i.e. EAPEVI1 and MDS1, in 3q26 are generated, resulting in the formation of a chimaeric transcription factor. The t(3;21) has only rarely been described in de novo leukaemias and never before in an acute leukaemia in a child. We here present the clinical, cytogenetic and molecular genetic findings in a boy with a de novo acute monoblastic leukaemia with t(3;21)(q26;q22) and AML1 rearrangement.

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