Expression of c-myb and B-myb oncogenes on myelofibrotic marrow fibroblasts

Leuk Lymphoma. 1999 Apr;33(3-4):295-304. doi: 10.3109/10428199909058429.

Abstract

The term IMF (Idiopathic Myelofibrosis) refers to a primary bone marrow disease in which the normal haematopoietic bone marrow cells are for unknown reasons replaced by connective tissue. The pathogenesis of the disease has not been clarified yet. We have speculated that the increment of proliferation of bone marrow fibroblasts in IMF may be the consequence of the over-expression of some oncogenes, leading or contributing to the fibrosis via a cell amplification. Thus, we investigated the possible role of the c-myb and B-myb genes in IMF and control bone marrow fibroblasts in different culture conditions to evaluate proliferation parameters in the absence or presence of serum. Using the reverse transcriptase polymerase chain reaction technique, we demonstrated that the kinetics of induction was similar for both c-myb and B-myb during the proliferation of normal bone marrow fibroblasts. When compared to normal controls, cultured IMF fibroblasts showed more elevated values of c-myb and B-myb RNA; furthermore, after a 72 hours stimulation with serum, c-myb and B-myb messages remained relatively high in myelofibrotic fibroblasts. Finally, after serum starvation, c-myb and to a lesser extent B-myb RNA levels remained unusually high in IMF fibroblasts, while under the same experimental conditions c-myb and B-myb messages became virtually undetectable in normal bone marrow fibroblasts. To our knowledge this work represents the first description of an abnormal behavior of these genes in IMF fibroblasts.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Bone Marrow / metabolism
  • Bone Marrow / pathology*
  • Cell Cycle Proteins*
  • Cell Division
  • Cells, Cultured
  • DNA-Binding Proteins / biosynthesis
  • DNA-Binding Proteins / genetics*
  • Female
  • Fibroblasts / metabolism
  • Fibroblasts / pathology
  • Humans
  • Kinetics
  • Liver / pathology
  • Male
  • Middle Aged
  • Oncogene Proteins / genetics
  • Primary Myelofibrosis / genetics
  • Primary Myelofibrosis / metabolism*
  • Primary Myelofibrosis / pathology*
  • Proto-Oncogene Proteins / biosynthesis
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins c-myb
  • Spleen / pathology
  • Trans-Activators / biosynthesis
  • Trans-Activators / genetics*

Substances

  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • MYBL2 protein, human
  • Oncogene Proteins
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-myb
  • Trans-Activators