Evidence map›Paper›PMID 25012565›Full record

Trial reportLeukemia research2014

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

Open access · greenAbstract readClinical Trial, Phase IIControlled Clinical TrialMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Leukemia research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. Osteosarcoma Overview.Rheumatology and therapy · 2017
    Review
  3. Review
  4. Type I interferons in anticancer immunity.Nature reviews. Immunology · 2015
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Joshua F ZeidnerDivision of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Douglas E GladstoneDivision of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Marianna ZahurakDivision of Oncology Biostatistics and Bioinformatics, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States.
William H MatsuiDivision of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Christopher GockeDepartment of Pathology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Richard J JonesDivision of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States.
B Douglas SmithDivision of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, United States. Electronic address: bdsmith@jhmi.edu.
Johns Hopkins University · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
ONCOLOGY: CHEMOTHERAPY, IMMUNOLOGY, BIOLOGYT32CA009071 · NCI · JOHNS HOPKINS UNIVERSITY · PI Mary Y Armanios, Nilofer S. Azad · 1985 to 2026
$12.8M
NCI NIH HHS P30 CA006973NCI NIH HHS P30CA006973NCI NIH HHS T32 CA009071NCI NIH HHS T32CA009071
6 · The paper itself

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.

Indexed as

AdultAgedAntineoplastic Combined Chemotherapy ProtocolsBenzamidesDrug SynergismFemaleGranulocyte-Macrophage Colony-Stimulating FactorHumansImatinib MesylateInterferon-alphaLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiddle AgedPiperazinesPyrimidinesRemission InductionBenzamidesGranulocyte-Macrophage Colony-Stimulating FactorImatinib MesylateInterferon-alphaPiperazinesPyrimidinesChronic myeloid leukemiaCureDiscontinuation of therapyGrowth factorsInterferonTyrosine kinase inhibitor

Identifiers

PMID25012565
PMCPMC4135379
OpenAlexW2072494396

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.