Imatinib and nilotinib inhibit hematopoietic progenitor cell growth, but do not prevent adhesion, migration and engraftment of human cord blood CD34+ cells

PLoS One. 2012;7(12):e52564. doi: 10.1371/journal.pone.0052564. Epub 2012 Dec 20.

Abstract

Background: The availability of tyrosine kinase inhibitors (TKIs) has considerably changed the management of Philadelphia chromosome positive leukemia. The BCR-ABL inhibitor imatinib is also known to inhibit the tyrosine kinase of the stem cell factor receptor, c-Kit. Nilotinib is 30 times more potent than imatinib towards BCR-ABL in vitro. Studies in healthy volunteers and patients with chronic myelogenous leukemia or gastrointestinal stromal tumors have shown that therapeutic doses of nilotinib deliver drug levels similar to those of imatinib. The aim of this study was to compare the inhibitory effects of imatinib and nilotinib on proliferation, differentiation, adhesion, migration and engraftment capacities of human cord blood CD34(+) cells.

Design and methods: After a 48-hour cell culture with or without TKIs, CFC, LTC-IC, migration, adhesion and cell cycle analysis were performed. In a second time, the impact of these TKIs on engraftment was assessed in a xenotransplantation model using NOD/SCID/IL-2Rγ (null) mice.

Results: TKIs did not affect LTC-IC frequencies despite in vitro inhibition of CFC formation due to inhibition of CD34(+) cell cycle entry. Adhesion of CD34(+) cells to retronectin was reduced in the presence of either imatinib or nilotinib but only at high concentrations. Migration through a SDF-1α gradient was not changed by cell culture in the presence of TKIs. Finally, bone marrow cellularity and human chimerism were not affected by daily doses of imatinib and nilotinib in a xenogenic transplantation model. No significant difference was seen between TKIs given the equivalent affinity of imatinib and nilotinib for KIT.

Conclusions: These data suggest that combining non-myeloablative conditioning regimen with TKIs starting the day of the transplantation could be safe.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, CD34 / metabolism*
  • Benzamides / pharmacology*
  • Cell Adhesion / drug effects
  • Cell Count
  • Cell Cycle / drug effects
  • Cell Movement / drug effects*
  • Cell Proliferation / drug effects
  • Colony-Forming Units Assay
  • Dose-Response Relationship, Drug
  • Fetal Blood / cytology*
  • Fetal Blood / transplantation*
  • Fibronectins / metabolism
  • Hematopoietic Stem Cells / cytology*
  • Hematopoietic Stem Cells / drug effects
  • Humans
  • Imatinib Mesylate
  • Integrin alpha4beta1 / metabolism
  • Integrin alpha5beta1 / metabolism
  • Mice
  • Models, Animal
  • Phosphorylation / drug effects
  • Piperazines / pharmacology*
  • Protein Kinase Inhibitors / pharmacology
  • Proto-Oncogene Proteins c-kit / metabolism
  • Pyrimidines / pharmacology*
  • Receptors, CXCR4 / metabolism
  • Recombinant Proteins / metabolism

Substances

  • Antigens, CD34
  • Benzamides
  • CXCR4 protein, human
  • Fibronectins
  • Integrin alpha4beta1
  • Integrin alpha5beta1
  • Piperazines
  • Protein Kinase Inhibitors
  • Pyrimidines
  • Receptors, CXCR4
  • Recombinant Proteins
  • retronectin
  • Imatinib Mesylate
  • Proto-Oncogene Proteins c-kit
  • nilotinib

Grants and funding

LB, F. Baron and YB have received travel grants from Novartis Pharmaceuticals. YB received unrestricted research grant from Novartis Pharmaceuticals. This does not alter the authors’ adherence to all the PLoS ONE policies on sharing data and materials. This study was supported by the National Fund for Scientific Research (FNRS; http://www1.frs-fnrs.be/). The travel grants and unrestricted research grants from Novartis Pharmaceuticals where not part of the funding for this study. The FNRS had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Similarly Novartis Pharmaceuticals had no role in study design, data collection and analysis or decision to publish. They did however receive the final draft of the publication prior to submission since they kindly provided the authors with imatinib and nilotinib, and suggested a number of minor edits to the manuscript.