Lack of involvement of T-lymphocytes in the leukaemic population during prolonged chronic phase of Philadelphia chromosome positive chronic myeloid leukaemia

Leuk Lymphoma. 1993 Jun;10(3):217-21. doi: 10.3109/10428199309145886.

Abstract

Nine patients with prolonged (> 2 years) chronic phase chronic myeloid leukaemia (CML) were investigated for the presence of T-cell involvement in the leukemic clone. Pure populations of peripheral blood T-cell populations were obtained by culturing separated mononuclear cells in the presence of pokeweed mitogen and IL2, until cultures showed > 99% pure T-cells. Purified T-cells and bone marrow and peripheral blood hematopoietic precursors were analysed for the presence of bcr-abl mRNA transcripts following RNA extraction and message amplification using polymerase chain reaction. In none of the 9 patients was bcr-abl mRNA found in T-lymphocytes while in all cases such transcripts were found in bone marrow and peripheral blood hematopoietic cells. Failure to detect T-cell involvement in patients with prolonged chronic phase CML using techniques designed to enhance even low level involvement of these cell populations supports the view that acquisition of the Ph chromosome abnormality does not occur in the totipotent stem cells but in more committed precursor cell/s with multilineage capacity but which only rarely retain the capacity for T-cell differentiation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biomarkers, Tumor / analysis
  • Biomarkers, Tumor / genetics
  • Blood Cells / pathology
  • Bone Marrow / pathology
  • Cell Differentiation
  • Clone Cells / pathology
  • Female
  • Fusion Proteins, bcr-abl / analysis
  • Fusion Proteins, bcr-abl / genetics
  • Humans
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology*
  • Leukemia, Myeloid, Chronic-Phase / pathology*
  • Male
  • Neoplastic Stem Cells / pathology
  • Polymerase Chain Reaction
  • T-Lymphocytes / pathology*

Substances

  • Biomarkers, Tumor
  • Fusion Proteins, bcr-abl