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

Research output: Contribution to journalArticle

Abstract

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
Volume38
Issue number8
DOIs
StatePublished - 2014

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Granulocyte-Macrophage Colony-Stimulating Factor
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Interferons
Cytogenetics
Protein-Tyrosine Kinases
Myeloid Progenitor Cells
Poisons
Intercellular Signaling Peptides and Proteins
Therapeutics

Keywords

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

ASJC Scopus subject areas

  • Cancer Research
  • Hematology
  • Oncology

Cite this

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title = "Granulocyte-macrophage colony stimulating factor (GM-CSF) enhances the clinical responses to interferon-α (IFN) in newly diagnosed chronic myeloid leukemia (CML)",
abstract = "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.",
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AU - Zeidner, Joshua F.

AU - Gladstone, Douglas

AU - Zahurak, Marianna

AU - Matsui, William H.

AU - Gocke, Christopher

AU - Jones, Richard J

AU - Smith, B Douglas

PY - 2014

Y1 - 2014

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AB - 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.

KW - Chronic myeloid leukemia

KW - Cure

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KW - Growth factors

KW - Interferon

KW - Tyrosine kinase inhibitor

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