Evidence map›Paper›PMID 26402671›Full record

ReviewInternational journal of molecular sciences2015

Pharmacogenetics of BCR/ABL Inhibitors in Chronic Myeloid Leukemia.

Marialuisa Polillo, Sara Galimberti, Claudia Baratè, Mario Petrini, Romano Danesi, Antonello Di Paolo

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

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  16. TheOncotarget · 2017
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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

6 authors at 1 institution in 1 country.

Marialuisa PolilloDepartment of Clinical and Experimental Medicine, Section of Pharmacology, University of Pisa, Via Roma 55, 56126 Pisa, Italy. polmarilu@yahoo.it.
Sara GalimbertiDepartment of Clinical and Experimental Medicine, Section of Hematology, University of Pisa, Via Roma 57, 56126 Pisa, Italy. sara.galimberti@med.unipi.it.
Claudia BaratèDepartment of Clinical and Experimental Medicine, Section of Hematology, University of Pisa, Via Roma 57, 56126 Pisa, Italy. claudia.barate@gmail.com.
Mario PetriniDepartment of Clinical and Experimental Medicine, Section of Hematology, University of Pisa, Via Roma 57, 56126 Pisa, Italy. mario.petrini@med.unipi.it.
Romano DanesiDepartment of Clinical and Experimental Medicine, Section of Pharmacology, University of Pisa, Via Roma 55, 56126 Pisa, Italy. romano.danesi@unipi.it.
Antonello Di PaoloDepartment of Clinical and Experimental Medicine, Section of Pharmacology, University of Pisa, Via Roma 55, 56126 Pisa, Italy. antonello.dipaolo@med.unipi.it.
University of Pisa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic myeloid leukemia was the first haematological neoplasia that benefited from a targeted therapy with imatinib nearly 15 years ago. Since then, several studies have investigated the role of genes, their variants (i.e., polymorphisms) and their encoded proteins in the pharmacokinetics and pharmacodynamics of BCR-ABL1 tyrosine kinase activity inhibitors (TKIs). Transmembrane transporters seem to influence in a significant manner the disposition of TKIs, especially that of imatinib at both cellular and systemic levels. In particular, members of the ATP-binding cassette (ABC) family (namely ABCB1 and ABCG2) together with solute carrier (SLC) transporters (i.e., SLC22A1) are responsible for the differences in drug pharmacokinetics. In the case of the newer TKIs, such as nilotinib and dasatinib, the substrate affinity of these drugs for transporters is variable but lower than that measured for imatinib. In this scenario, the investigation of genetic variants as possible predictive markers has led to some discordant results. With the partial exception of imatinib, these discrepancies seem to limit the application of discovered biomarkers in the clinical settings. In order to overcome these issues, larger prospective confirmative trials are needed.

Indexed as

PharmacogeneticsAnimalsATP-Binding Cassette TransportersBiological TransportDrug Resistance, NeoplasmFusion Proteins, bcr-ablHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveOrganic Cation Transport ProteinsProtein Kinase InhibitorsATP-Binding Cassette TransportersFusion Proteins, bcr-ablOrganic Cation Transport ProteinsProtein Kinase Inhibitorsbosutinibchronic myeloid leukemiadasatinibimatinibnilotinibpharmacogeneticspharmacogenomicsponatinibtransmembrane transporter

Identifiers

PMID26402671
PMCPMC4613337
OpenAlexW2142593918

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.