Acute myelogenous leukaemia

The incidence of acute myelogenous leukaemia (AML) increases steadily with age, more than 50% of the cases being diagnosed in subjects aged 60 years or over [1,2]. Age has been reported as an adverse prognostic indicator in AML affecting both remission rates and survival [1–3]. The overall unsatisfactory therapeutic results appear related to either host-related factors, (the impaired capacity of older patients to tolerate the toxic effects of dose-intense chemotherapy), and intrinsic differences in the biology of leukaemia itself (Table 1) [4,5]. First, AML in the elderly displays clonal involvement not only at level of the granulomonocytic lineage, as for most of de novo adult AMLs, but also erythroid and megakaryocytic progenitors are often involved [5]. These findings, along with the very frequent expression of the CD34 antigen, suggest that AML in older persons probably originates from a more primitive multipotent stem cell [5,6]. The multilineage involvement and the resulting functional impairment of the residual normal stem cell pool, might account for the reported longer duration of post-chemotherapy aplasia and for the increased risk of induction deaths in the elderly AML [2–5]. Second, unfavourable karyotypic abnormalities are more frequently detected in elderly than in younger AML patients, along with a low frequency of favourable cytogenetic patterns [5–7]. Third, the incidence of AML secondary to a preceding myelodysplastic syndrome (MDS), or the presence of bone marrow tri-lineage dysplastic changes in apparently de novo AMLs, are very elevated in older patients [1–5]. This fact carries an important prognostic significance since, independently from age, AMLs developing after MDS have a high rate of primary resistance to chemotherapy [4,5]. Fourth, FAB cytotypes associated with a poor prognosis (M1, M5 and M6), display a