Evidence map›Paper›PMID 26556869›Full record

ArticleOncotarget2015

Phenotypic profile of expanded NK cells in chronic lymphoproliferative disorders: a surrogate marker for NK-cell clonality.

Paloma Bárcena, María Jara-Acevedo, María Dolores Tabernero, Antonio López, María Luz Sánchez, Andrés C García-Montero, Noemí Muñoz-García, María Belén Vidriales, Artur Paiva, Quentin Lecrevisse and 6 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 30 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

16 authors at 7 institutions in 3 countries.

Paloma BárcenaCancer Research Centre (IBMCC, CSIC-USAL), Institute of Biomedical Research of Salamanca (IBSAL), (NUCLEUS) and Department of Medicine, University of Salamanca, Salamanca, Spain.
María Jara-AcevedoCancer Research Centre (IBMCC, CSIC-USAL), Institute of Biomedical Research of Salamanca (IBSAL), (NUCLEUS) and Department of Medicine, University of Salamanca, Salamanca, Spain.
María Dolores TaberneroResearch Unity and IECSCYL, University Hospital of Salamanca and IBSAL, Salamanca, Spain.
Antonio LópezCancer Research Centre (IBMCC, CSIC-USAL), Institute of Biomedical Research of Salamanca (IBSAL), (NUCLEUS) and Department of Medicine, University of Salamanca, Salamanca, Spain.
María Luz SánchezCancer Research Centre (IBMCC, CSIC-USAL), Institute of Biomedical Research of Salamanca (IBSAL), (NUCLEUS) and Department of Medicine, University of Salamanca, Salamanca, Spain.
Andrés C García-MonteroCancer Research Centre (IBMCC, CSIC-USAL), Institute of Biomedical Research of Salamanca (IBSAL), (NUCLEUS) and Department of Medicine, University of Salamanca, Salamanca, Spain.
Noemí Muñoz-GarcíaCancer Research Centre (IBMCC, CSIC-USAL), Institute of Biomedical Research of Salamanca (IBSAL), (NUCLEUS) and Department of Medicine, University of Salamanca, Salamanca, Spain.
María Belén VidrialesDepartment of Hematology and Institute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, Salamanca, Spain.
Artur PaivaUnidade de Gestão Operacional em Citometria, Serviço de Patologia Clínica, Centro Hospitalar e Universitário de Coimbra, Instituto Politécnico de Coimbra, ESTESC-Coimbra Health School, Análises Clínicas e Saúde Pública, Coimbra,Portugal.
Quentin LecrevisseCancer Research Centre (IBMCC, CSIC-USAL), Institute of Biomedical Research of Salamanca (IBSAL), (NUCLEUS) and Department of Medicine, University of Salamanca, Salamanca, Spain.
Margarida LimaDepartment of Hematology, Laboratory of Cytometry, Hospital de Santo António, Centro Hospitalar do Porto, and Unit for Multidisciplinary Research in Biomedicine (UMIB), Porto, Portugal.
Anton W LangerakDepartment of Immunology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
Sebastian BöttcherMedical Clinic II, University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Jacques J M van DongenDepartment of Immunology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
Alberto OrfaoCancer Research Centre (IBMCC, CSIC-USAL), Institute of Biomedical Research of Salamanca (IBSAL), (NUCLEUS) and Department of Medicine, University of Salamanca, Salamanca, Spain.
Julia AlmeidaCancer Research Centre (IBMCC, CSIC-USAL), Institute of Biomedical Research of Salamanca (IBSAL), (NUCLEUS) and Department of Medicine, University of Salamanca, Salamanca, Spain.
Centro de Investigación del Cáncer · ESInstituto de Investigación Biomédica de Salamanca · ESErasmus MC · NLUniversidad de Salamanca · ESCentro Hospitalar do Porto · PTInstituto de Estudios de Ciencias de la Salud de Castilla y León · ESPolytechnic Institute of Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Currently, the lack of a universal and specific marker of clonality hampers the diagnosis and classification of chronic expansions of natural killer (NK) cells. Here we investigated the utility of flow cytometric detection of aberrant/altered NK-cell phenotypes as a surrogate marker for clonality, in the diagnostic work-up of chronic lymphoproliferative disorders of NK cells (CLPD-NK). For this purpose, a large panel of markers was evaluated by multiparametric flow cytometry on peripheral blood (PB) CD56(low) NK cells from 60 patients, including 23 subjects with predefined clonal (n = 9) and polyclonal (n = 14) CD56(low) NK-cell expansions, and 37 with CLPD-NK of undetermined clonality; also, PB samples from 10 healthy adults were included. Clonality was established using the human androgen receptor (HUMARA) assay. Clonal NK cells were found to show decreased expression of CD7, CD11b and CD38, and higher CD2, CD94 and HLADR levels vs. normal NK cells, together with a restricted repertoire of expression of the CD158a, CD158b and CD161 killer-associated receptors. In turn, NK cells from both clonal and polyclonal CLPD-NK showed similar/overlapping phenotypic profiles, except for high and more homogeneous expression of CD94 and HLADR, which was restricted to clonal CLPD-NK. We conclude that the CD94(hi)/HLADR+ phenotypic profile proved to be a useful surrogate marker for NK-cell clonality.

Indexed as

AdultAgedAged, 80 and overBiomarkersChronic DiseaseClone CellsCluster AnalysisFemaleFlow CytometryHumansImmunophenotypingKiller Cells, NaturalLymphoproliferative DisordersMiddle AgedPhenotypeReceptors, AndrogenAR protein, humanBiomarkersReceptors, AndrogenclonalityCLPD-NKimmunophenotypenatural killer cellsNK cells

Identifiers

PMID26556869
PMCPMC4767482
OpenAlexW2239617171

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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.