Evidence map›Paper›PMID 31900171›Full record

ArticleJournal of translational medicine2020

Flow cytometry and targeted immune transcriptomics identify distinct profiles in patients with chronic myeloid leukemia receiving tyrosine kinase inhibitors with or without interferon-α.

Raquel Alves, Stephanie E B McArdle, Jayakumar Vadakekolathu, Ana Cristina Gonçalves, Paulo Freitas-Tavares, Amélia Pereira, Antonio M Almeida, Ana Bela Sarmento-Ribeiro, Sergio Rutella

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 22 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

9 authors at 5 institutions in 2 countries.

Raquel AlvesLaboratory of Oncobiology and Hematology and University Clinic of Hematology/Faculty of Medicine, University of Coimbra (FMUC), Coimbra, Portugal.
Stephanie E B McArdleJohn van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Campus, Nottingham, NG11 8NS, UK.
Jayakumar VadakekolathuJohn van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Campus, Nottingham, NG11 8NS, UK.
Ana Cristina GonçalvesLaboratory of Oncobiology and Hematology and University Clinic of Hematology/Faculty of Medicine, University of Coimbra (FMUC), Coimbra, Portugal.
Paulo Freitas-TavaresClinical Hematology Department, Centro Hospitalar Universitário de Coimbra (CHUC), Coimbra, Portugal.
Amélia PereiraCoimbra Institute for Clinical and Biomedical Research (iCBR) - Group of Environment Genetics and Oncobiology (CIMAGO), FMUC, Coimbra, Portugal.
Antonio M AlmeidaHospital da Luz, Lisbon, Portugal.
Ana Bela Sarmento-RibeiroLaboratory of Oncobiology and Hematology and University Clinic of Hematology/Faculty of Medicine, University of Coimbra (FMUC), Coimbra, Portugal.
Sergio RutellaJohn van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Campus, Nottingham, NG11 8NS, UK. sergio.rutella@ntu.ac.uk.ORCID 0000-0003-1970-7375
Nottingham Trent University · GBHospitais da Universidade de Coimbra · PTUniversity of Coimbra · PTCelulose Beira Industrial (Portugal) · PTUniversidade Católica Portuguesa · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumor cells have evolved complex strategies to escape immune surveillance, a process which involves NK cells and T lymphocytes, and various immunological factors. Indeed, tumor cells recruit immunosuppressive cells [including regulatory T-cells (Treg), myeloid-derived suppressor cells (MDSC)] and express factors such as PD-L1. Molecularly targeted therapies, such as imatinib, have off-target effects that may influence immune function. Imatinib has been shown to modulate multiple cell types involved in anti-cancer immune surveillance, with potentially detrimental or favorable outcomes. Imatinib and other tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML) have dramatically changed disease course. Our study aimed to characterize the different populations of the immune system in patients with CML affected by their treatment.

methodsForty-one patients with CML [33 treated with TKIs and 8 with TKIs plus interferon (IFN)-α] and 20 controls were enrolled in the present study. Peripheral blood populations of the immune system [referred to as the overview of immune system (OVIS) panel, Treg cells and MDSCs] and PD-1 expression were evaluated by flow cytometry. The immunological profile was assessed using the mRNA Pan-Cancer Immune Profiling Panel and a NanoString nCounter FLEX platform.

resultsPatients receiving combination therapy (TKIs + IFN-α) had lower numbers of lymphocytes, particularly T cells [838/µL (95% CI 594-1182)] compared with healthy controls [1500/µL (95% CI 1207 - 1865), p = 0.017]. These patients also had a higher percentage of Treg (9.1%) and CD4

conclusionsOur results suggest that TKIs in combination with IFN-α may promote an enhanced immune suppressive state.

Indexed as

Interferon-alphaLeukemia, Myelogenous, Chronic, BCR-ABL PositiveFlow CytometryHumansProtein Kinase InhibitorsTranscriptomeInterferon-alphaProtein Kinase InhibitorsChronic myeloid leukemiaGene expression profilingImmune monitoringImmunotherapyInterferon

Identifiers

PMID31900171
PMCPMC6941328
OpenAlexW2999674042

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.