title: Mesenchymal stem cells in patients with chronic myelogenous leukaemia or bi-phenotypic Ph+ acute leukaemia are not related to the leukaemic clone.
abstract: BACKGROUND
  Human mesenchymal stem cells (MSCs) are thought to be multipotent cells which primarily reside in the bone marrow. Besides their well-known ability to replicate as undifferentiated cells and to differentiate into diverse lineages of mesenchymal tissues, they were recently suggested to also give rise to haematopoietic and leukaemic/cancer stem cells. In this study, the relationship between MSCs and leukemic stem cells in patients with either chronic myelogenous leukaemia (CML) or the more primitive variant, Ph+ bi-phenotypic leukaemia was investigated.
  
  
  METHODS
  Cultured MSCs from 5 patients with CML and 3 patients with bi-phenotypic Ph+ leukaemia, all of them positive for BCP-ABL, were analysed with conventional cytogenetics, fluorescence in situ hybridisation (FISH) and polymerase chain reaction (PCR) for the presence of t(9;22) and BCR-ABL. MSCs were characterised phenotypically with surface markers (+CD73, +CD90, +CD105, -CD34, -CD45) and functionally through their potential to differentiate into both adipocytes and osteoblasts.
  
  
  RESULTS
  MSCs could be cultivated from seven patients. These cells were BCR-ABL negative when analysed with conventional cytogenetics and FISH. Further cytogenetic analysis revealed a normal set of chromosomes without any aberrations. Two patients were BCR-ABL-positive when analysed with PCR, probably as a result of MSC contamination with macrophages.
  
  
  CONCLUSIONS
  MSCs in patients with CML or Ph+ bi-phenotypic leukaemia are not related to the malignant cell clone.
authors.affiliation: Department of Internal Medicine 1, Division of Bone Marrow Transplantation, Medical University of Vienna, Vienna, Austria. swoehrer@bccrc.ca
authors.forename: S
authors.initials: S
authors.lastname: Wöhrer
authors.forename: W
authors.initials: W
authors.lastname: Rabitsch
authors.forename: M
authors.initials: M
authors.lastname: Shehata
authors.forename: R
authors.initials: R
authors.lastname: Kondo
authors.forename: H
authors.initials: H
authors.lastname: Esterbauer
authors.forename: B
authors.initials: B
authors.lastname: Streubel
authors.forename: C
authors.initials: C
authors.lastname: Sillaber
authors.forename: M
authors.initials: M
authors.lastname: Raderer
authors.forename: U
authors.initials: U
authors.lastname: Jaeger
authors.forename: C
authors.initials: C
authors.lastname: Zielinski
authors.forename: P
authors.initials: P
authors.lastname: Valent
mesh_terms: D048708:Cell Growth Processes / Q000502:physiology; D002869:Chromosome Aberrations; D016044:Fusion Proteins, bcr-abl / Q000235:genetics; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics / Q000473:pathology*; D059630:Mesenchymal Stem Cells / Q000473:pathology*; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: C406060:abl-bcr fusion protein, human; D016044:Fusion Proteins, bcr-abl