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.
authors.affiliation: Division of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States.
authors.forename: Joshua F
authors.initials: JF
authors.lastname: Zeidner
authors.affiliation: Division of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States.
authors.forename: Douglas E
authors.initials: DE
authors.lastname: Gladstone
authors.affiliation: Division of Oncology Biostatistics and Bioinformatics, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States.
authors.forename: Marianna
authors.initials: M
authors.lastname: Zahurak
authors.affiliation: Division of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States.
authors.forename: William H
authors.initials: WH
authors.lastname: Matsui
authors.affiliation: Department of Pathology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States.
authors.forename: Christopher
authors.initials: C
authors.lastname: Gocke
authors.affiliation: Division of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States.
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Jones
authors.affiliation: Division of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States. Electronic address: bdsmith@jhmi.edu.
authors.forename: B Douglas
authors.initials: BD
authors.lastname: Smith
mesh_terms: D000328:Adult; D000368:Aged; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use*; D001549:Benzamides / Q000627:therapeutic use; D004357:Drug Synergism; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000008:administration & dosage*; D006801:Humans; D000068877:Imatinib Mesylate; D016898:Interferon-alpha / Q000008:administration & dosage*; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D010879:Piperazines / Q000627:therapeutic use; D011743:Pyrimidines / Q000627:therapeutic use; D012074:Remission Induction; D055815:Young Adult
chemical_list: D001549:Benzamides; D016898:Interferon-alpha; D010879:Piperazines; D011743:Pyrimidines; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D000068877:Imatinib Mesylate
keywords: Chronic myeloid leukemia; Cure; Discontinuation of therapy; Growth factors; Interferon; Tyrosine kinase inhibitor