Experimental hematology · 2004
DNA microarray analysis of dysplastic morphology associated with acute myeloid leukemia.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Tsutsumi Chizuko, Ueda Masuzu, Miyazaki Yasushi, Yamashita Yoshihiro, Choi Young Lim, Ota Jun, Kaneda Ruri, Koinuma Koji, Fujiwara Shin-ichiro, Kisanuki Hiroyuki, Ishikawa Madoka, Ozawa Keiya, Tomonaga Masao, Mano Hiroyuki
Аннотация
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.
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.