Evidence map›Paper›PMID 14523461›Full record

Trial reportLeukemia2003

Imatinib produces significantly superior molecular responses compared to interferon alfa plus cytarabine in patients with newly diagnosed chronic myeloid leukemia in chronic phase.

S Branford, Z Rudzki, A Harper, A Grigg, K Taylor, S Durrant, C Arthur, P Browett, A P Schwarer, D Ma and 6 more

Abstract readClinical TrialClinical Trial, Phase IIIComparative Study
PubMed Publisher
In one paragraph

Trial report in Leukemia, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.

  1. Chronic Myelogenous Leukemia, Version 1.2014.Journal of the National Comprehensive Cancer Network : JNCCN · 2013
    Guideline
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. [How I treat pediatric chronic myeloid leukemia].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. BCR-ABL1 tyrosine kinase inhibitors for the treatment of chronic myeloid leukemia.Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners · 2018
    Review
  16. Article
  17. Article
  18. Molecular monitoring.Current hematologic malignancy reports · 2014
    Review
  19. Article
  20. Article
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

16 authors at 13 institutions in 3 countries.

S BranfordInstitute of Medical and Veterinary Science, Adelaide, South Australia.
Z Rudzki
A Harper
A Grigg
K Taylor
S Durrant
C Arthur
P Browett
A P Schwarer
D Ma
J F Seymour
K Bradstock
D Joske
K Lynch
I Gathmann
T P Hughes
South Australia Pathology · AUAuckland City Hospital · NZMater Adult Hospital · AUNovartis (Australia) · AUNovartis (Switzerland) · CHPeter MacCallum Cancer Centre · AURoyal Brisbane and Women's Hospital · AURoyal North Shore Hospital · AUSir Charles Gairdner Hospital · AUSt Vincent's Hospital Melbourne · AUThe Alfred Hospital · AUThe Royal Melbourne Hospital · AUWestmead Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We analyzed molecular responses in 55 newly diagnosed chronic-phase chronic myeloid leukemia (CML) patients enrolled in a phase 3 study (the IRIS trial) comparing imatinib to interferon-alfa plus cytarabine (IFN+AraC). BCR-ABL/BCR% levels were measured by real-time quantitative RT-PCR and were significantly lower for the imatinib-treated patients at all time points up to 18 months, P<0.0001. The median levels for imatinib-treated patients continued to decrease and had not reached a plateau by 24 months. A total of 24 IFN+AraC-treated patients crossed over to imatinib. Once imatinib commenced, the median BCR-ABL/BCR% levels in these patients were not significantly different to those on first-line imatinib for the equivalent number of months. The incidence of progression in imatinib-treated patients, defined by hematologic, cytogenetic or quantitative PCR criteria, was significantly higher in the patients who failed to achieve a 1 log reduction by 3 months or a 2 log reduction by 6 months, P=0.002. A total of 49 patients were screened for BCR-ABL kinase domain mutations. Mutations were detected in two imatinib-treated patients who crossed over from IFN+AraC and both lost their imatinib response. In conclusion, first-line imatinib-treated patients had profound reductions in BCR-ABL/BCR%, which significantly exceeded those of IFN+AraC-treated patients and early measurements were predictive of subsequent response.

Indexed as

Antimetabolites, AntineoplasticAntineoplastic AgentsBenzamidesBone MarrowCross-Over StudiesCytarabineCytogeneticsDNA Mutational AnalysisFusion Proteins, bcr-ablHumansImatinib MesylateInterferon-alphaLeukemia, Myelogenous, Chronic, BCR-ABL PositivePhosphotransferasesPiperazinesPrognosisAntimetabolites, AntineoplasticAntineoplastic AgentsBenzamidesCytarabineFusion Proteins, bcr-ablImatinib MesylateInterferon-alphaPhosphotransferasesPiperazinesPyrimidines

Identifiers

PMID14523461
OpenAlexW1988399039

What OpenQuestion holds

Textmetadata
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.