Acute myeloid leukemia : distinctive chromosome abnormalities in patients treated with pipobroman or hydroxyurea

ET is a chronic myeloproliferative disorder rarely evolving into AML, sometimes preceded by a myelodysplastic syndrome (MDS). Such transformations mostly occur in patients treated with radiophosphorous ([sup.32]P) or alkylating agents, especially busulfan. Recently, concern has also arisen about the...

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Published inLeukemia Vol. 16; no. 10; p. 2078
Main Authors Bernasconi, P, Boni, M, Cavigliano, P.M, Calatroni, S, Brusamolino, E, Passamonti, F, Volpe, G, Pistorio, A, Giardini, I, Rocca, B, Caresana, M, Lazzarino, M, Bernasconi, C
Format Journal Article
LanguageEnglish
Published Nature Publishing Group 01.10.2002
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Summary:ET is a chronic myeloproliferative disorder rarely evolving into AML, sometimes preceded by a myelodysplastic syndrome (MDS). Such transformations mostly occur in patients treated with radiophosphorous ([sup.32]P) or alkylating agents, especially busulfan. Recently, concern has also arisen about the longterm safety of hydroxyurea (HU). Pipobroman (PI), a well tolerated and simple to use drug, constitutes a valid alternative to those cytoreductive treatments. The present study reports on 155 ET patients treated at our institution from 1985 to 1995, and monitored until December 2000. A good control of thrombocytosis was achieved with PI as the only treatment in 106 patients and with HU in 23 patients. Twenty-six patients received no treatment. After a median follow-up of 104 months, seven patients (four treated with HU, and three with PI) developed AML whereas one patient treated with PI developed MDS. A significant difference in progression-free survival was observed between HU- and PI-treated patients (P = 0.004). A short-arm deletion of chromosome 17 was most frequently detected in HU-treated patients, while a long-arm trisomy of chromosome 1 and a monosomy 7q were seen in PI-treated patients. No TP53 mutation was discovered in the six patients studied (two HU-treated and four PI-treated). We conclude that these cytogenetic abnormalities are not linked to the natural history of the disease, but rather that they might be induced by the cytoreductive treatment. Leukemia (2002) 16, 2078-2083. doi:10.1038/sj.leu.2402638 Keywords: cytogenetics; FISH; chromosome abnormalities; 17p-; TP53
ISSN:0887-6924
1476-5551