Evidence map›Paper›PMID 23238589›Full record

ReviewLeukemia2013

Re-emergence of interferon-α in the treatment of chronic myeloid leukemia.

M Talpaz, R Hehlmann, A Quintás-Cardama, J Mercer, J Cortes

Open access · hybridAbstract readReview
In one paragraph

Review in Leukemia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 2% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
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  5. Trial
  6. Review
  7. Natural and Engineered Cytokines as Cancer Therapeutics.Annual review of cancer biology · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. An Overview of Advances in Rare Cancer Diagnosis and Treatment.International journal of molecular sciences · 2024
    Review
  12. Review
  13. Article
  14. Treatment of CML in pregnancy.Hematology. American Society of Hematology. Education Program · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

10 more citing papers are in PubMed but not listed here.

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

5 authors at 4 institutions in 2 countries.

M TalpazDepartment of Internal Medicine, Division of Hematology Oncology, University of Michigan Comprehensive Cancer Center, Ann Arbor, MI 48109-5936, USA. mtalpaz@med.umich.edu
R Hehlmann
A Quintás-Cardama
J Mercer
J Cortes
The University of Texas MD Anderson Cancer Center · USMedizinische Fakultät MannheimMichigan Medicine · USUniversity of Michigan–Ann Arbor · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Treatment for chronic myeloid leukemia (CML) has evolved from chemotherapy (busulfan, hydroxyurea) to interferon-α (IFNα), and finally to tyrosine kinase inhibitors such as imatinib. Although imatinib has profoundly improved outcomes for patients with CML, it has limitations. Most significantly, imatinib cannot eradicate CML primitive progenitors, which likely accounts for the high relapse rate when imatinib is discontinued. IFNα, unlike imatinib, preferentially targets CML stem cells. Early studies with IFNα in CML demonstrated its ability to induce cytogenetic remission. Moreover, a small percentage of patients treated with IFNα were able to sustain durable remissions after discontinuing therapy and were probably cured. The mechanisms by which IFNα exerts its antitumor activity in CML are not well understood; however, activation of leukemia-specific immunity may have a role. Some clinical studies have demonstrated that the combination of imatinib and IFNα is superior to either therapy alone, perhaps because of their different mechanisms of action. Nonetheless, the side effects of IFNα often impede its administration, especially in combination therapy. Here, we review the role of IFNα in CML treatment and the recent developments that have renewed interest in this once standard therapy for patients with CML.

Indexed as

HumansInterferon-alphaLeukemia, Myelogenous, Chronic, BCR-ABL PositiveNeoplasm, ResidualInterferon-alpha

Identifiers

PMID23238589
PMCPMC3703612
OpenAlexW1991917484

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.