Gene expression profiling of myelodysplastic CD34+ hematopoietic stem cells treated in vitro with decitabine

Leuk Res. 2011 Apr;35(4):465-71. doi: 10.1016/j.leukres.2010.07.022.

Abstract

Abnormal gene promoter methylation contributes to deregulate gene expression of hematopoietic progenitors in myelodysplastic syndromes (MDS). We analyzed the gene expression profile of myelodysplastic and normal CD34+ hematopoietic stem cells (HSCs) treated in vitro with decitabine. We identified a list of candidate tumor suppressor genes, expressed at low levels in MDS HSCs and induced by hypomethylating treatment only in MDS, but not in normal HSCs. Real-time RT-PCR confirmed reduced CD9 expression in MDS CD34+ and bone marrow mononuclear cells, compared to normal controls. CD9 was specifically up-regulated by decitabine treatment in myelodysplastic CD34+ cells.

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Antigens, CD34 / blood
  • Antimetabolites, Antineoplastic / pharmacology
  • Azacitidine / analogs & derivatives*
  • Azacitidine / pharmacology
  • Cluster Analysis
  • DNA Methylation
  • Decitabine
  • Female
  • Gene Expression / drug effects
  • Gene Expression Profiling*
  • Hematopoietic Stem Cells / drug effects*
  • Hematopoietic Stem Cells / metabolism
  • Humans
  • Integrin beta1 / genetics
  • Male
  • Middle Aged
  • Myelodysplastic Syndromes / blood
  • Myelodysplastic Syndromes / genetics*
  • Oligonucleotide Array Sequence Analysis
  • Promoter Regions, Genetic / genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • Young Adult

Substances

  • Antigens, CD34
  • Antimetabolites, Antineoplastic
  • Integrin beta1
  • Decitabine
  • Azacitidine

Associated data

  • GEO/GSE19610