Hyperdiploidy with a chromosome number between 51 and 65 and a mean peak at 55 occurs as a distinct karyotype pattern in approximately 25-30% of ALLs in childhood [1, 2]. It is considered a favorable prognostic factor. The most intriguing cytogenetic peculiarities of these leukemias are the nearly exclusive presence of nonrandom numerical abnormalities due to the gain of chromosomes 4, 6, 10, 14, 17, 18, 20, 21 and X [1, 2]. In contrast, chromosomes 1, 2, 3, 12 and 16 are rarely involved [1,

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... Typically, the affected chromosomes are present in three copies, with chromosome 21 also often being tetrasomic.Near-haploid cases, on the other hand, are extremely rare and have a bad prognosis [1, 2]. They contain at least one copy of each chromosome, a second copy of one of the sex chromosomes and both chromosomes 21 in most instances. In addition, two copies of chromosomes 10, 14 and 18 are commonly found.In the majority of cases of hyperdiploid ALL, the mechanism leading to the increased number of chromosomes is unknown. However, once formed, the abnormal karyotype is uniform and stable in the malignant cell population. Molecular genetic studies performed by Onodera et al. [3] revealed that the hyperdiploid karyotype usually arises by a simultaneous event during a single abnormal cell division from a diploid karyotype. Occasionally, this can also occur by doubling of the chromosomes from a near-haploid karyotype [4]. In virtually all cases, tetrasomy of chromosome 21 was generated by a duplication of both the maternally and paternally derived homolog. This finding was one of the main arguments for the notion that hyperdiploidy cannot be caused by stepwise or sequential gains from a diploid karyotype or by consecutive losses from a tetraploid karyotype.