Evidence map›Paper›PMID 27519478›Full record

ArticleJournal of translational medicine2016

Role of KIR and CD16A genotypes in colorectal carcinoma genetic risk and clinical stage.

Angelica Canossi, Anna Aureli, Tiziana Del Beato, Piero Rossi, Luana Franceschilli, Flavio De Sanctis, Pierpaolo Sileri, Nicola di Lorenzo, Oreste Buonomo, Davide Lauro and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 13 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

12 authors at 2 institutions in 1 country.

Angelica CanossiLaboratory of Tumor Immunology and Immunotherapy, CNR Institute of Translational Pharmacology (IFT), Via Fosso del Cavaliere 100, 00133, L'Aquila, Rome, Italy.
Anna AureliLaboratory of Tumor Immunology and Immunotherapy, CNR Institute of Translational Pharmacology (IFT), Via Fosso del Cavaliere 100, 00133, L'Aquila, Rome, Italy.
Tiziana Del BeatoLaboratory of Tumor Immunology and Immunotherapy, CNR Institute of Translational Pharmacology (IFT), Via Fosso del Cavaliere 100, 00133, L'Aquila, Rome, Italy.
Piero RossiDepartment of Experimental Medicine and Surgery, University of Rome Tor Vergata, Rome, Italy.
Luana FranceschilliDepartment of Experimental Medicine and Surgery, University of Rome Tor Vergata, Rome, Italy.
Flavio De SanctisDepartment of Experimental Medicine and Surgery, University of Rome Tor Vergata, Rome, Italy.
Pierpaolo SileriDepartment of Experimental Medicine and Surgery, University of Rome Tor Vergata, Rome, Italy.
Nicola di LorenzoDepartment of Experimental Medicine and Surgery, University of Rome Tor Vergata, Rome, Italy.
Oreste BuonomoDepartment of Experimental Medicine and Surgery, University of Rome Tor Vergata, Rome, Italy.
Davide LauroDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Adriano VendittiDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
Giuseppe SconocchiaLaboratory of Tumor Immunology and Immunotherapy, CNR Institute of Translational Pharmacology (IFT), Via Fosso del Cavaliere 100, 00133, L'Aquila, Rome, Italy. giuseppe.sconocchia@cnr.it.ORCID 0000-0003-3260-4856
University of Rome Tor Vergata · ITIstituto di Farmacologia Traslazionale · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNK cell cytotoxicity is regulated by the types of the interaction between killer immunoglobulin-like receptors (KIRs) and human leukocyte antigen (HLA) class I ligands on target cells and the different binding affinity of the Fcγ receptor IIIA (CD16A) for IgG-coated tumor cells. Thus, it is conceivable that KIR and CD16A gene contents may contribute to the function of NK cells by modulating an immune response in the colorectal carcinoma (CRC) microenvironment. This hypothesis is supported by recent evidence suggesting that NK cells improve the clinical course of CRC patients by enhancing the anti-CRC effect of CD8 + T cells. This information provides the rationale to test the hypothesis whether the independent KIR segregation and specificity, as well as CD16A gene polymorphisms, have an impact on CRC.

methodsUsing polymerase chain reaction-sequence-specific primers (PCR-SSP) and sequence-based typing (SBT), we investigated KIR/HLA-C complex and CD16A (48H/R/L,158V/F) gene polymorphisms in 52 CRC patients and 61 local healthy controls (LCTRs).

resultsThe allele frequency (AF) of at least five activating KIR (aKIRs) of the B haplotype (p = 0.036, OR 0.204), KIR2DL2 (p = 0.047, OR 0.2616), and KIR2DS2 genes (5.8 vs LCTR 13.8 % and vs. Fasano's CTR 16.3 %, p = 0.05, OR 0.3145), in the absence of their cognate HLA-C1 ligands, were significantly associated with a reduced genetic risk of CRC. In contrast, CD16A-48H polymorphism was positively associated with an increased genetic risk of CRC (p = 0.05, OR 2.761). The latter was also found to be correlated with advanced stages of disease [III and IV (p = 0.03, OR 3.625)].

conclusionsOur data suggest that the analysis of aKIRs and KIR2DL2 gene and CD16A-48H may be of interest for the identification of individuals at reduced and increased genetic risk of CRC, respectively.

Indexed as

Genetic Predisposition to DiseaseAgedAllelesCase-Control StudiesColorectal NeoplasmsDemographyFemaleGene FrequencyGenetic Association StudiesGenotypeHaplotypesHLA-C AntigensHumansItalyLigandsMaleFCGR3A protein, humanHLA-C AntigensLigandsReceptors, IgGReceptors, KIRCD16AColorectal carcinomaCRCFCGR3A genotypesGenetic riskKIRNK

Identifiers

PMID27519478
PMCPMC4983069
OpenAlexW2513344154

What OpenQuestion holds

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LicenceCC BY
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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.