Summary. During a 10-year period (1992)(1993)(1994)(1995)(1996)(1997)(1998)(1999)(2000)(2001) in the region of Southern Denmark, 337 patients aged 15 years or older (range 16-93 years, median 67 years) were diagnosed with acute myeloid leukaemia (AML). Cytogenetic analysis was carried out in 90%, of whom 53% had clonal chromosome aberrations. Some 24% and 31% had only numerical or structural abnormalities respectively. The remaining patients showed both types of abnormalities. Ploidy levels in decreasing order were: pseudodiploidy, 41%; hyperdiploidy, 32%; and hypodiploidy, 27%. Pseudodiploidy characterizes type M3 (70%) and hypodiploidy M6 (56%). Recurrent cytogenetic abnormalities -t(8;21), t(15;17) and inv(16) -were found in 3AE3%, 3AE3% and 2AE0% of all patients respectively. Prognostically intermediate and adverse aberrations were found in 39% and 44%, respectively, of those with an abnormal karyotype. Rare recurrent aberrations were found in two patients in this material. A previously described non-recurrent abnormality was found to be recurrent in one patient [der(20)t(11;20)(q13.2;p13)]. New, previously undescribed abnormalities were found in 41 patients. Statistically significant correlations were found between t(15;17) and young age (P < 0AE001), inv(16) and young age (P < 0AE006), )17 and M6 (P ¼ 0AE007), and M6 and complex karyotype with five or more unrelated aberrations (P ¼ 0AE004). We conclude that this truely population-based cytogenetic study of adult AML showed distributions of chromosome abnormalities that differ from those described so far.Keywords: acute myeloid leukaemia, adults, cytogenetics, population based.Since 1976, when the first French-American-British (FAB) classification was published (Bennett et al, 1976), the subclassification of acute myeloid leukaemia (AML) has been based on cell morphology. In 1988, the Morphologic, Immunologic and Cytogenetic (MIC) classification was published (Second MIC Cooperative Study Group, 1988) and, since then, cytogenetic investigations have become more and more important in AML classification (Grimwade et al, 1998). The detection of recurrent non-random chromosomal abnormalities resulted in a new understanding of AML, subdividing the disease into true de novo (TDN)-AML including patients with t(8;21), t(15;17), inv(16), t(16;16), t(9;11), t(11;17), t(6;9), t(1;22) and t(8;16), and myelodysplastic syndrome related (MDR)-AML including patients with )5, 5q-, )7, 7q-, +8, 11q-, inv(3) and translocations involving 3q (Head, 1996). This model was incorporated in the latest World Health Organization (WHO) classification, which divides AML into four major categories: (1) AML with recurrent genetic abnormalities [t(8;21), t(15;17), inv(16) and 11q23 abnormalities]; (2) AML with multilineage dysplasia; (3) therapy-related AML; and (4) AML not otherwise categorized (including FAB subtypes M0-M7) (Jaffe et al, 2001).Many papers have been published describing the frequencies, correlations to FAB subtypes and prognostic significance of non-random chromosomal ab...

No abstract

No abstract

No abstract

No abstract