Evidence map›Paper›PMID 28902850›Full record

ArticlePloS one2017

Copy number variation analysis in cytochromes and glutathione S-transferases may predict efficacy of tyrosine kinase inhibitors in chronic myeloid leukemia.

Alexander V Lavrov, Oksana A Ustaeva, Elmira P Adilgereeva, Svetlana A Smirnikhina, Ekaterina Y Chelysheva, Oleg A Shukhov, Yuriy V Shatokhin, Sergey V Mordanov, Anna G Turkina, Sergey I Kutsev

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Alexander V LavrovLaboratory of Mutagenesis, Federal State Budgetary Institution Research Centre for Medical Genetics, Moscow, Russian Federation.
Oksana A UstaevaLaboratory of Medical Genetics, The Rostov State Medical University, Rostov-on-Don, Russian Federation.
Elmira P AdilgereevaLaboratory of Mutagenesis, Federal State Budgetary Institution Research Centre for Medical Genetics, Moscow, Russian Federation.
Svetlana A SmirnikhinaLaboratory of Mutagenesis, Federal State Budgetary Institution Research Centre for Medical Genetics, Moscow, Russian Federation.ORCID http://orcid.org/0000-0002-1558-3048
Ekaterina Y ChelyshevaScientific and Advisory Department of Chemotherapy of Myeloproliferative disorders, Federal State-Funded Institution National Research Center for Hematology of the Ministry of Healthcare of the Russian Federation, Moscow, Russian Federation.
Oleg A ShukhovScientific and Advisory Department of Chemotherapy of Myeloproliferative disorders, Federal State-Funded Institution National Research Center for Hematology of the Ministry of Healthcare of the Russian Federation, Moscow, Russian Federation.
Yuriy V ShatokhinLaboratory of Medical Genetics, The Rostov State Medical University, Rostov-on-Don, Russian Federation.
Sergey V MordanovLaboratory of Medical Genetics, The Rostov State Medical University, Rostov-on-Don, Russian Federation.
Anna G TurkinaScientific and Advisory Department of Chemotherapy of Myeloproliferative disorders, Federal State-Funded Institution National Research Center for Hematology of the Ministry of Healthcare of the Russian Federation, Moscow, Russian Federation.
Sergey I KutsevLaboratory of Mutagenesis, Federal State Budgetary Institution Research Centre for Medical Genetics, Moscow, Russian Federation.
Ministry of Health of the Russian Federation · RURostov State Medical University · RUResearch Centre for Medical Genetics · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) is a myeloproliferative disease characterized by the presence of BCR/ABL fusion gene in leukemic cells, which promotes uncontrolled cell proliferation. Up to 20% of CML patients show primary resistance or non-optimal response to tyrosine kinase inhibitor (TKI) therapy. We investigated the association between copy number variation (CNV) in glutathione S-transferases (GST) and cytochromes (CYP) and the response rate to TKI. We enrolled 47 patients with CML: 31 with an optimal response and 16 with failure at 6 months in accordance with European LeukemiaNet 2013 recommendations. CNV detection was performed using SALSA MLPA P128-C1 Cytochrome P450 probe mix. Patients with optimal response and with failure of TKI therapy showed different frequencies of wild type and mutated CYPs and GST (p<0.0013). Validation in the group of 15 patients proved high prognostic value (p = 0.02): positive and negative predictive value 83% and 78%; sensitivity and specificity 71% and 88%. Wild type genotypes of CYP and GST associate with a worse response to TKI treatment in CML patients. This test can be recommended for further clinical trials.

Indexed as

DNA Copy Number VariationsAdultAgedBiomarkers, TumorCase-Control StudiesCytochromesDrug Resistance, NeoplasmFemaleGlutathione TransferaseHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiddle AgedPrognosisProtein Kinase InhibitorsTreatment OutcomeBiomarkers, TumorCytochromesGlutathione TransferaseProtein Kinase Inhibitors

Identifiers

PMID28902850
PMCPMC5597128
OpenAlexW2755082526

What OpenQuestion holds

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LicenceCC BY
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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.