Correspondence:

Therapy-related myelodysplastic syndrome/acute myeloid leukemia (t-MDS/AML) is an increasingly recognized treatment complication in patients treated with radiothera-py or chemotherapy for previous hematologic malignancies or solid tumors. Distinct clinical entities have been described according to the primary treatment, correspon-ding to defined genetic lesions. Chromosome 7 and/or 5 losses or deletions are typ-ical of alkylating agent-induced AML, while development of t-AML with balanced translocations involving chromosome bands 11q23 and 21q22 has been related to previous therapy with drugs targeting DNA-topoisomerase II. In addition, anti-metabo-lites, and in particular the immunosuppressant azathioprine, have been shown to induce defective DNA-mismatch repair. This could promote survival of misrepaired cells giving rise to the leukemic clone. Individual predisposing factors, including poly-morphisms in detoxification and DNA repair enzymes have been identified. Their com-bination may significantly increase the risk of t-MDS/AML. Among patients with hema-tologic malignancies, long-term survivors of Hodgkin’s lymphoma are exposed to an increased risk of t-MDS/AML, particularly when receiving MOPP-based, and escalate