DNA microarray analysis of dysplastic morphology associated with acute myeloid leukemia

Objective Acute myeloid leukemia (AML) develops de novo or secondarily to either myelodysplastic syndrome (MDS) or anticancer treatment (therapy-related leukemia, TRL). Prominent dysplasia of blood cells is apparent in individuals with MDS-related AML as well as in some patients with TRL or even with de novo AML. The clinical entity of AML with multilineage dysplasia (AML-MLD) is likely to be an amalgamation of MDS-related AML and de novo AML-MLD. The aim of this study was to clarify, by the use of high-density oligonucleotide microarrays, whether these subcategories of AML are intrinsically distinct from each other. Materials and Methods The AC133 + hematopoietic stem cell–like fractions were purified from the bone marrow of individuals with de novo AML without dysplasia (n=15), AML-MLD (n=11), MDS-related AML (n=11), or TRL (n=2), and were subjected to the synthesis of cRNA which was subsequently hybridized to microarray harboring oligonucleotide corresponding to more than 12,000 probe sets. Results We could identify many genes whose expression was specific to these various subcategories of AML. Furthermore, with the correspondence analysis/three-dimensional projection strategy, we were able to visualize the independent, yet partially overlapping, nature of current AML subcategories on the basis of their transcriptomes. Conclusion Our data indicate the possibility of subclassification of AML based on gene expression profiles of leukemic blasts.