Evidence map›Paper›PMID 37647275›Full record

ArticlePloS one2023

Evaluation of KIR3DL1/KIR3DS1 allelic polymorphisms in Kenyan children with endemic Burkitt lymphoma.

Beatrice M Muriuki, Catherine S Forconi, Erastus K Kirwa, Titus K Maina, Bonface O Ariera, Jeffrey A Bailey, Anita Ghansah, Ann M Moormann, John M Ong'echa

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

Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 65% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. Review
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 4 institutions in 3 countries.

Beatrice M MuriukiWest African Center for Cell Biology of Infectious Pathogens, College of Basic and Applied Sciences, University of Ghana, Accra, Ghana.ORCID 0000-0001-9824-8706
Catherine S ForconiDivision of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Chan Medical School, Worcester, MA, United States of America.
Erastus K KirwaCenter for Global Health Research, Kenya Medical Research Institute, Kisumu, Kenya.
Titus K MainaCenter for Global Health Research, Kenya Medical Research Institute, Kisumu, Kenya.
Bonface O ArieraCenter for Global Health Research, Kenya Medical Research Institute, Kisumu, Kenya.
Jeffrey A BaileyDepartment of Pathology and Laboratory Medicine, Warren Alpert Medical School, Brown University, Providence, RI, United States of America.
Anita GhansahNoguchi Memorial Institute for Medical Research, College of Health Sciences, University of Ghana, Legon, Accra, Ghana.ORCID 0000-0003-4639-1249
Ann M MoormannDivision of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Chan Medical School, Worcester, MA, United States of America.
John M Ong'echaCenter for Global Health Research, Kenya Medical Research Institute, Kisumu, Kenya.ORCID 0000-0003-3928-6774
Kenya Medical Research Institute · KEUniversity of Ghana · GHUniversity of Massachusetts Chan Medical School · USBrown University · US

Funding

Impact of malaria on shaping immunity to EBV in the etiology of Burkitt lymphomaR01CA189806 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MOORMANN, ANN M · 2014 to 2024
$5.7M
NCI NIH HHS R01 CA189806Wellcome TrustWellcome Trust 107755/Z/15/Z:
6 · The paper itself

Abstract

Endemic Burkitt lymphoma (eBL) is a fast-growing germinal center B cell lymphoma, affecting 5-10 per 100,000 children annually, in the equatorial belt of Africa. We hypothesize that co-infections with Plasmodium falciparum (Pf) malaria and Epstein-Barr virus (EBV) impair host natural killer (NK) and T cell responses to tumor cells, and thus increase the risk of eBL pathogenesis. NK cell education is partially controlled by killer immunoglobulin-like receptors and variable expression of KIR3DL1 has been associated with other malignancies. Here, we investigated whether KIR3D-mediated mechanisms contribute to eBL, by testing for an association of KIR3DL1/KIR3DS1 genotypes with the disease in 108 eBL patients and 99 healthy Kenyan children. KIR3DL1 allelic typing and EBV loads were assessed by PCR. We inferred previously observed phenotypes from the genotypes. The frequencies of KIR3DL1/KIR3DL1 and KIR3DL1/KIR3DS1 did not differ significantly between cases and controls. Additionally, none of the study participants was homozygous for KIR3DS1 alleles. EBV loads did not differ by the KIR3DL1 genotypes nor were they different between eBL survivors and non-survivors. Our results suggest that eBL pathogenesis may not simply involve variations in KIR3DL1 and KIR3DS1 genotypes. However, considering the complexity of the KIR3DL1 locus, this study could not exclude a role for copy number variation in eBL pathogenesis.

Indexed as

Burkitt LymphomaEpstein-Barr Virus InfectionsMalaria, FalciparumAllelesDNA Copy Number VariationsHerpesvirus 4, HumanHumansKenyaReceptors, KIR3DL1Receptors, KIR3DS1KIR3DL1 protein, humanKIR3DS1 protein, humanReceptors, KIR3DL1Receptors, KIR3DS1

Identifiers

PMID37647275
PMCPMC10468049
OpenAlexW4386275729

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.