Absence of mutations in the granulocyte colony-stimulating factor (G-CSF) receptor gene in patients with myelodysplastic syndrome/acute myeloblastic leukaemia occurring after treatment of aplastic anaemia with G-CSF

Br J Haematol. 2000 Nov;111(2):656-8. doi: 10.1046/j.1365-2141.2000.02370.x.

Abstract

The development of myelodysplastic syndrome/acute myeloblastic leukaemia (MDS/AML) has been reported in patients with aplastic anaemia (AA) after administration of recombinant human granulocyte colony-stimulating factor (rhG-CSF). Similarly, patients with severe congenital neutropenia (SCN) have an increased risk of developing MDS/AML after treatment with rhG-CSF. Point mutations in the G-CSF receptor gene are found in about 20% of SCN patients who are predisposed to MDS/AML. We investigated the occurrence of mutations in the G-CSF receptor in eight patients with AA who developed MDS/AML. No mutations were detected around the cytoplasmic domain of the gene in our patients, indicating that the mechanisms of clonal evolution to MDS/AML in patients with AA might be different from those with SCN.

MeSH terms

  • Adult
  • Anemia, Aplastic / drug therapy*
  • Child
  • Child, Preschool
  • Granulocyte Colony-Stimulating Factor / therapeutic use*
  • Humans
  • Immunosuppressive Agents / therapeutic use*
  • Leukemia, Myeloid, Acute / etiology*
  • Male
  • Myelodysplastic Syndromes / etiology*
  • Point Mutation
  • Polymorphism, Single-Stranded Conformational
  • Receptors, Granulocyte Colony-Stimulating Factor / genetics*
  • Recombinant Proteins

Substances

  • Immunosuppressive Agents
  • Receptors, Granulocyte Colony-Stimulating Factor
  • Recombinant Proteins
  • Granulocyte Colony-Stimulating Factor