Molecular and functional analysis of the stem cell compartment of chronic myelogenous leukemia reveals the presence of a CD34- cell population with intrinsic resistance to imatinib

Blood. 2009 Dec 10;114(25):5191-200. doi: 10.1182/blood-2008-08-176016.

Abstract

We show the molecular and functional characterization of a novel population of lineage-negative CD34-negative (Lin(-)CD34(-)) hematopoietic stem cells from chronic myelogenous leukemia (CML) patients at diagnosis. Molecular karyotyping and quantitative analysis of BCR-ABL transcript demonstrated that approximately one-third of CD34(-) cells are leukemic. CML Lin(-)CD34(-) cells showed kinetic quiescence and limited clonogenic capacity. However, stroma-dependent cultures induced CD34 expression on some cells and cell cycling, and increased clonogenic activity and expression of BCR-ABL transcript. Lin(-)CD34(-) cells showed hematopoietic cell engraftment rate in 2 immunodeficient mouse strains similar to Lin-CD34(+) cells, whereas endothelial cell engraftment was significantly higher. Gene expression profiling revealed the down-regulation of cell-cycle arrest genes and genes involved in antigen presentation and processing, while the expression of genes related to tumor progression, such as angiogenic factors, was strongly up-regulated compared with normal counterparts. Phenotypic analysis confirmed the significant down-regulation of HLA class I and II molecules in CML Lin(-)CD34(-) cells. Imatinib mesylate did not reduce fusion transcript levels, BCR-ABL kinase activity, and clonogenic efficiency of CML Lin(-)CD34(-) cells in vitro. Moreover, leukemic CD34(-) cells survived exposure to BCR-ABL inhibitors in vivo. Thus, we identified a novel CD34(-) leukemic stem cell subset in CML with peculiar molecular and functional characteristics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, CD34 / metabolism*
  • Antineoplastic Agents / pharmacology
  • Benzamides
  • Bone Marrow Cells / metabolism
  • Cells, Cultured
  • Cluster Analysis
  • Drug Resistance, Neoplasm*
  • Flow Cytometry
  • Fusion Proteins, bcr-abl / genetics
  • Gene Expression Profiling
  • Humans
  • Imatinib Mesylate
  • Interleukin Receptor Common gamma Subunit / deficiency
  • Interleukin Receptor Common gamma Subunit / genetics
  • Karyotyping
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism*
  • Mice
  • Mice, Inbred NOD
  • Mice, Knockout
  • Mice, SCID
  • Neoplastic Stem Cells / metabolism*
  • Neoplastic Stem Cells / pathology
  • Neoplastic Stem Cells / transplantation
  • Oligonucleotide Array Sequence Analysis
  • Piperazines / pharmacology*
  • Pyrimidines / pharmacology*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transplantation, Heterologous
  • beta 2-Microglobulin / deficiency
  • beta 2-Microglobulin / genetics

Substances

  • Antigens, CD34
  • Antineoplastic Agents
  • Benzamides
  • Il2rg protein, mouse
  • Interleukin Receptor Common gamma Subunit
  • Piperazines
  • Pyrimidines
  • beta 2-Microglobulin
  • Imatinib Mesylate
  • Fusion Proteins, bcr-abl

Associated data

  • GEO/GSE11675