Epigenetic-based treatments emphasize the biologic differences of core-binding factor acute myeloid leukemias

Elena Serrano, Maria J. Carnicer, Adriana Lasa, Vanesa Orantes, Jorge Pena, Salut Brunet, Anna Aventín, Jorge Sierra, Josep F. Nomdedéu

Research output: Contribution to journalArticleResearchpeer-review

6 Citations (Scopus)

Abstract

Acute myeloid leukemia (AML) is a heterogeneous group of disorders characterized by an abnormal proliferation of the myeloid precursors and a maturation block. The most common chromosomal lesions in AML are the t(8;21) and inv(16). To better understand the leukemogenic mechanism of these fusion proteins, we performed gene expression studies in samples from (8;21), AML1 mutated and inv(16) patients, as well as from the Kasumi-1 cell line and a U937 cell line expressing the AML1-ETO fusion gene. To assess the influence of associated epigenetic lesions, we performed gene expression studies in Kasumi-1 cells and cells extracted from an Inv(16) patient, both treated with demethylating and HDAC inhibitor agents. Shared deregulated genes in the different types of core-binding factor leukemias were identified. We found a tight link between Inv(16) and mutant AML1 samples. Furthermore, some of the genes deregulated by the leukemogenic process reverted to their normal expression with demethylating and HDAC inhibitor treatment, highlighting the role of chromatin remodeling processes in AML. © 2007 Elsevier Ltd. All rights reserved.
Original languageEnglish
Pages (from-to)944-953
JournalLeukemia Research
Volume32
DOIs
Publication statusPublished - 1 Jun 2008

Keywords

  • AML1 gene mutation
  • AML1-ETO fusion gene
  • Acute myeloid leukemia
  • Expression profiling
  • Microarrays

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