Granulocyte-macrophage colony stimulating factor (GM-CSF) enhances the clinical responses to interferon-α (IFN) in newly diagnosed chronic myeloid leukemia (CML)

Joshua F. Zeidner, Douglas E. Gladstone, Marianna Zahurak, William H. Matsui, Christopher Gocke, Richard J. Jones, B. Douglas Smith

Research output: Contribution to journalArticle


The majority of chronic myeloid leukemia (CML) patients treated with tyrosine kinase inhibitors (TKIs) remain with residual disease. In contrast to TKIs, interferon (IFN) is directly toxic to CML progenitor cells, and myeloid growth factors such as GM-CSF may enhance IFN's cytotoxicity. We performed a phase 2 study of IFN. +. GM-CSF in 58 newly diagnosed CML patients before imatinib approval. Short-term clinical responses included: 60% major cytogenetic response, 28% complete cytogenetic response and 19% complete molecular response. Six patients remain off all therapy for CML (range: 15 months-12 years) after IFN. +. GM-CSF treatment. IFN. +. GM-CSF shows promise as an adjunctive therapy for CML.

Original languageEnglish (US)
Pages (from-to)886-890
Number of pages5
JournalLeukemia Research
Issue number8
StatePublished - Aug 2014



  • Chronic myeloid leukemia
  • Cure
  • Discontinuation of therapy
  • Growth factors
  • Interferon
  • Tyrosine kinase inhibitor

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

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