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Studies of the nuclear architecture have concluded that chromosomes 8 and 21 tend to colocalize in myeloid cells. Tissue-specific genomic organization probably contributes to the formation of this disease-specific translocation. This is also supported by studies of umbilical cord leukocytes that have described an association between prenatal pesticide exposure (i.e., detection of pesticides in meconium) and the detection of t(8 21) in the leukocytes and the level of the fusion transcript then correlated with the pesticide level. The detection of t(8 21) transcripts in Guthrie cards suggests that the initiating events can occur in utero. Approximately 10%вЂ“20% of children with AML have this translocation. The incidence of AML with favourable cytogenetic abnormalities decreases with age this is also true for t(8 21) that is most common in children/younger patients and uncommon in patients above 60 years of age. The t(8 21) abnormality is found in approximately 5%вЂ“10% of all AML cases and 10%вЂ“22% of AML cases with maturation corresponding to the previous FAB class M2. The t(8 21) Abnormality in Human AML 2.1. In the present paper we describe the biology and clinical characteristics of the most common t(8 21) abnormality. been reported to be involved in 39 different rearrangements and most of them have been detected in myeloid malignancies. t(8 21) was the first cytogenetic abnormality discovered in AML, and today it offers a unique example of how a cytogenetic abnormality is used to define a distinct subgroup of patients.

The criteria for the diagnosis differs from other AML patients the leukemia cells showbiological characteristics that are uncommon in other AML subsets, and the prognosis after intensive chemotherapy is better for these patients than for the majority of AML patients. The translocation fuses the AML1 gene (also called RUNX1) on chromosome 21 with the ETO gene (also referred to as the RUNX1T1 gene that encodes the CBFA2T1 protein) on chromosome 8.

IntroductionДЄcute myeloid leukemia (AML) is a heterogeneous bone marrow malignancy, and patients with the cytogenetic t(8 21) abnormality represent a subset with specific clinical and biological characteristics. To conclude, detection of t(8 21) is essential for optimal handling of these patients as it has both diagnostic, prognostic, and therapeutic implications. Whether the detection of the fusion gene can be used for evaluation of minimal residual disease and risk of leukemia relapse remains to be clarified. t(8 21) is usually associated with a good prognosis. If t(8 21) is detected in a patient with bone marrow pathology, the diagnosis AML can be made based on this abnormality alone. The translocation can be detected as the only genetic abnormality or as part of more complex abnormalities. This protein has multiple effects on the regulation of the proliferation, the differentiation, and the viability of leukemic cells. The translocation results in an in-frame fusion of two genes, resulting in a fusion protein of one N-terminal domain from the AML1 gene and four C-terminal domains from the ETO gene. The t(8 21) abnormality occurs in a minority of acute myeloid leukemia (AML) patients.

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