Rapid detection of phosphotyrosine proteins by flow cytometric analysis in Bcr-Abl-positive cells

Cytometry A. 2004 Nov;62(1):35-45. doi: 10.1002/cyto.a.20030.

Abstract

Background: Constitutive tyrosine phosphorylation derived from Bcr-Abl kinase activity is the major characteristic of Bcr-Abl positive cells. In this study, we developed a method to detect the phosphotyrosine proteins by flow cytometry and we asked whether phosphorylation was affected by imatinib mesylate treatment.

Methods: Cells were treated or not with imatinib mesylate, fixed and permeabilized by PFA followed by saponin, then stained with anti-phosphotyrosine (p-tyr) monoclonal antibody and analyzed by flow cytometry.

Results: Optimal staining parameters were performed with p-tyr antibody using K562 and LAMA84 lines that displayed high levels of tyrosine phosphorylation as compared to the control line, HL60. Tyrosine phosphorylation was inhibited by imatinib in a dose-dependent manner, but not modified by other inhibitors demonstrating that the staining detected is specific to Bcr-Abl phosphorylation. The staining of imatinib-resistant cell lines such as the mutated BaF/Bcr-AblT315I cell line or resistant CML patient cells, showed that hyperphosphorylation was not affected by imatinib treatment. In one CML patient, our technique permitted us to detect a small hyperphosphorylated population resistant to imatinib that appeared hyperphosphorylated and amplified at the time of relapse.

Conclusions: We have developed a flow cytometric technique presenting several advantages such as rapidity and sensitivity, which requires fewer cells than the Western blot.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Benzamides
  • Biomarkers, Tumor / metabolism
  • Bone Marrow Cells / drug effects
  • Bone Marrow Cells / pathology
  • Cell Line, Tumor
  • Cell Separation / methods
  • Dose-Response Relationship, Drug
  • Drug Resistance, Neoplasm / drug effects
  • Flow Cytometry / methods*
  • Fusion Proteins, bcr-abl / analysis
  • Fusion Proteins, bcr-abl / metabolism*
  • Humans
  • Imatinib Mesylate
  • Intracellular Signaling Peptides and Proteins / pharmacology
  • Intracellular Signaling Peptides and Proteins / therapeutic use*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • Leukocytes, Mononuclear / drug effects
  • Leukocytes, Mononuclear / pathology
  • Mice
  • Phosphorylation
  • Phosphotyrosine / analysis
  • Phosphotyrosine / metabolism*
  • Piperazines / pharmacology
  • Piperazines / therapeutic use*
  • Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Pyrimidines / pharmacology
  • Pyrimidines / therapeutic use*

Substances

  • Benzamides
  • Biomarkers, Tumor
  • Intracellular Signaling Peptides and Proteins
  • Piperazines
  • Pyrimidines
  • protein kinase modulator
  • Phosphotyrosine
  • Imatinib Mesylate
  • Protein-Tyrosine Kinases
  • Fusion Proteins, bcr-abl