Evidence map›Paper›PMID 25245580›Full record

SynthesisThe pharmacogenomics journal2015

ABCB1 polymorphisms predict imatinib response in chronic myeloid leukemia patients: a systematic review and meta-analysis.

Q Zheng, H Wu, Q Yu, D H Dennis Kim, J H Lipton, S Angelini, S Soverini, D Vivona, N Takahashi, J Cao

Abstract readMeta-AnalysisSystematic Review
PubMed Publisher
In one paragraph

Synthesis in The pharmacogenomics journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Frontiers in pharmacology · 2021
    Article
  11. Article
  12. Review
  13. Pharmacology of tyrosine kinase inhibitors in chronic myeloid leukemia; a clinician's perspective.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2020
    Review
  14. Article
  15. Germline variants in cancer therapy.Cancer drug resistance (Alhambra, Calif.) · 2019
    Review
  16. Review
  17. Review
  18. Blood advances · 2017
    Article
  19. Article
  20. Pharmacogenomics and personalized medicine · 2017
    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

10 authors.

Q ZhengClinical Research Center, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
H WuDepartment of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Q YuDepartment of Surgical Oncology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
D H Dennis KimChronic Myelogenous Leukemia Group, Princess Margaret Cancer Centre, University Health Network University of Toronto, Toronto, Ontario, Canada.
J H LiptonChronic Myelogenous Leukemia Group, Princess Margaret Cancer Centre, University Health Network University of Toronto, Toronto, Ontario, Canada.
S AngeliniDepartment of Pharmacy and Biotechnology, University of Bologna, Bologna, Italy.
S SoveriniDepartment of Experimental, Diagnostic and Specialty Medicine, Institute of Hematology, University of Bologna, Bologna, Italy.
D VivonaDepartmento de Análises Clínicas e Toxicológicas da Faculdade de Ciências Farmacêuticas da Universidade de São Paulo, São Paulo, Brazil.
N TakahashiDepartment of Hematology, Nephrology, and Rheumatology, Akita University Graduate School of Medicine, Akita, Japan.
J CaoClinical Research Center, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Imatinib mesylate, a competitive tyrosine kinase inhibitor, is considered the first-line therapy drug for Ph+ chronic myeloid leukemia (CML). Three single-nucleotide polymorphisms (SNPs) in the ATP-binding cassette, subfamily B (MDR/TAP), member 1 gene (ABCB1/MDR1), c.1236C>T, c.2677G>T/A and c.3435C>T, have been shown to affect cellular transport/metabolism of imatinib. The associations between these SNPs and imatinib response in CML patients have been widely evaluated, but the results were inconsistent. To derive a conclusive assessment of the associations, we performed a meta-analysis by combining data from a total of 12 reports including 1826 patients. The results showed that the 2677G allele or 3435T allele predicted a worse response to imatinib in CML patients, whereas 1236CC genotype was associated with better response in CML patients from Asian region. In conclusion, this meta-analysis suggests that c.1236C>T, c.2677G>T/A and c.3435C>T can be served as predictive markers for the therapeutical use of imatinib in CML patients.

Indexed as

AdolescentAdultAgedAged, 80 and overAllelesAsian PeopleATP Binding Cassette Transporter, Subfamily BChildChild, PreschoolGene FrequencyGenotypeHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMiddle AgedPolymorphism, Single NucleotideABCB1 protein, humanATP Binding Cassette Transporter, Subfamily BImatinib MesylateProtein Kinase Inhibitors

Identifiers

PMID25245580

What OpenQuestion holds

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Registered trials

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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.