During the last three decades it has become apparent that the majority of c
ases of acute myeloid leukaemia (AML) are characterized by at least one of
a variety of recurrent chromosomal abnormalities. These changes have been f
ound in many instances to correlate closely with distinct morphological fea
tures and clinical characteristics, the molecular basis of which is becomin
g increasingly understood. Furthermore, diagnostic karyotype has been shown
to be a key determinant of outcome in AML, with mounting evidence to suppo
rt the notion that cytogenetic analysis can serve to identify biologically
distinct subsets of disease that demand tailored therapeutic approaches. Th
is has led to a rising trend towards routine cytogenetic and molecular char
acterization of newly diagnosed acute leukaemia, providing a framework for
treatment stratification.