Evidence map›Paper›PMID 27635733›Full record

ArticleBlood cancer journal2016

MATE1 regulates cellular uptake and sensitivity to imatinib in CML patients.

S Harrach, C Schmidt-Lauber, T Pap, H Pavenstädt, E Schlatter, E Schmidt, W E Berdel, U Schulze, B Edemir, S Jeromin and 3 more

Open access · goldAbstract read
In one paragraph

Article in Blood cancer journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  5. Interaction of Masitinib with Organic Cation Transporters.International journal of molecular sciences · 2022
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  6. Pharmacogenomics in Psychiatry Practice: The Value and the Challenges.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Review
  9. Development, validation, and application of an LC-MS/MS method for the determination of the AXL/FLT3 inhibitor gilteritinib in mouse plasma.Journal of chromatography. B, Analytical technologies in the biomedical and life sciences · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. 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

13 authors at 3 institutions in 1 country.

S HarrachInstitute of Experimental Musculoskeletal Medicine, University Hospital Münster, Münster, Germany.
C Schmidt-LauberExperimental Nephrology, Medizinische Klinik D, University Hospital Münster, Münster, Germany.
T PapInstitute of Experimental Musculoskeletal Medicine, University Hospital Münster, Münster, Germany.
H PavenstädtMolecular Nephrology, Department of Internal Medicine D, University Hospital Münster, Münster, Germany.
E SchlatterExperimental Nephrology, Medizinische Klinik D, University Hospital Münster, Münster, Germany.
E SchmidtDepartment of Medicine A, University Hospital Münster, Münster, Germany.
W E BerdelDepartment of Medicine A, University Hospital Münster, Münster, Germany.
U SchulzeMolecular Nephrology, Department of Internal Medicine D, University Hospital Münster, Münster, Germany.
B EdemirClinic and Polyclinic of Internal Medicine IV, Hematology and Oncology, University Hospital Halle, Halle (Saale), Germany.
S JerominMLL Munich Leukemia Laboratory, München, Germany.
T HaferlachMLL Munich Leukemia Laboratory, München, Germany.
G CiarimboliExperimental Nephrology, Medizinische Klinik D, University Hospital Münster, Münster, Germany.
J BertrandInstitute of Experimental Musculoskeletal Medicine, University Hospital Münster, Münster, Germany.
University Hospital Münster · DEMunich Leukemia Laboratory (Germany) · DEUniversity Hospital in Halle · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although imatinib is highly effective in the treatment of chronic myeloid leukemia (CML), 25-30% patients do not respond or relapse after initial response. Imatinib uptake into targeted cells is crucial for its molecular response and clinical effectiveness. The organic cation transporter 1 (OCT1) has been proposed to be responsible for this process, but its relevance has been discussed controversially in recent times. Here we found that the multidrug and toxin extrusion protein 1 (MATE1) transports imatinib with a manifold higher affinity. MATE1 mainly mediates the cellular uptake of imatinib into targeted cells and thereby controls the intracellular effectiveness of imatinib. Importantly, MATE1 but not OCT1 expression is reduced in total bone marrow cells of imatinib-non-responding CML patients compared with imatinib-responding patients, indicating that MATE1 but not OCT1 determines the therapeutic success of imatinib. We thus propose that imatinib non-responders could be identified early before starting therapy by measuring MATE1 expression levels.

Indexed as

Drug Resistance, NeoplasmAdultAgedAntineoplastic AgentsCell Line, TumorFemaleFusion Proteins, bcr-ablGene ExpressionGene Knockdown TechniquesHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiddle AgedOrganic Cation Transporter 1Organic Cation Transport ProteinsAntineoplastic AgentsFusion Proteins, bcr-ablImatinib MesylateOrganic Cation Transporter 1Organic Cation Transport ProteinsProtein Kinase InhibitorsSLC47A1 protein, human

Identifiers

PMID27635733
PMCPMC5056971
OpenAlexW2520700653

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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.