Evidence map›Paper›PMID 26268853›Full record

ArticleThe Journal of infectious diseases2016

Risk of Classic Kaposi Sarcoma With Combinations of Killer Immunoglobulin-Like Receptor and Human Leukocyte Antigen Loci: A Population-Based Case-control Study.

James J Goedert, Maureen P Martin, Francesco Vitale, Carmela Lauria, Denise Whitby, Ying Qi, Xiaojiang Gao, Mary Carrington

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

Article in The Journal of infectious diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Trial
  2. The Role of Killer Ig-like Receptors in Diseases from A to Z.International journal of molecular sciences · 2025
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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

8 authors at 2 institutions in 2 countries.

James J GoedertDivision of Cancer Epidemiology and Genetics, Division of Cancer Epidemiology and Genetics, National Cancer Institute.
Maureen P MartinCancer and Inflammation Program, Laboratory of Experimental Immunology Ragon Institute of MGH, MIT, and Harvard, Cambridge, Massachusetts.
Francesco VitaleDipartimento di Igiene e Microbiologia Giuseppe D'Alessandro, Universitá degli Studi di Palermo.
Carmela LauriaLega Italiana per la Lotta Contro i Tumori-Sez Ragusa, Italy.
Denise WhitbyViral Oncology Section, AIDS and Cancer Virus Program, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Maryland.
Ying QiCancer and Inflammation Program, Laboratory of Experimental Immunology Ragon Institute of MGH, MIT, and Harvard, Cambridge, Massachusetts.
Xiaojiang GaoCancer and Inflammation Program, Laboratory of Experimental Immunology Ragon Institute of MGH, MIT, and Harvard, Cambridge, Massachusetts.
Mary CarringtonCancer and Inflammation Program, Laboratory of Experimental Immunology Ragon Institute of MGH, MIT, and Harvard, Cambridge, Massachusetts.
Ragon Institute of MGH, MIT and Harvard · USLega Italiana per la Lotta ai Tumori · IT

Funding

Microbes and Human MalignanciesZIACP010214 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI VOGTMANN, EMILY · 2010 to 2021
$5.5M
CCR NIH HHS HHSN261200800001CIntramural NIH HHS ZIA CP010214NCI NIH HHS HHSN261200800001E
6 · The paper itself

Abstract

backgroundKaposi sarcoma (KS) is a complication of KS-associated herpesvirus (KSHV) infection. Other oncogenic viral infections and malignancies are associated with certain HLA alleles and their natural killer (NK) cell immunoglobulin-like receptor (KIR) ligands. We tested whether HLA-KIR influences the risk of KSHV infection or KS.

methodsIn population-based case-control studies, we compared HLA class I and KIR gene frequencies in 250 classic (non-AIDS) KS cases, 280 KSHV-seropositive controls, and 576 KSHV-seronegative controls composing discovery and validation cohorts. Logistic regression was used to calculate sex- and age-adjusted odds ratios (ORs) and 95% confidence intervals.

resultsIn both the discovery and validation cohorts, KS was associated with HLA-A*11:01 (adjusted OR for the combined cohorts, 0.4; P = .002) and HLA-C*07:01 (adjusted OR, 1.6; P = .002). Consistent associations across cohorts were also observed with activating KIR3DS1 plus HLA-B Bw4-80I and homozygosity for HLA-C group 1. With KIR3DS1 plus HLA-B Bw4-80I, the KSHV seroprevalence was 40% lower (adjusted OR for the combined cohorts, 0.6; P = .01), but the KS risk was 2-fold higher (adjusted OR, 2.1; P = .002). Similarly, the KSHV seroprevalence was 40% lower (adjusted OR, 0.6; P = .01) but the KS risk 80% higher with HLA-C group 1 homozygosity (adjusted OR, 1.8; P = .005).

conclusionsKIR-mediated NK cell activation may decrease then risk of KSHV infection but enhance KSHV dissemination and progression to KS if infection occurs.

Indexed as

Herpesvirus 8, HumanCase-Control StudiesGene Expression RegulationGenetic Predisposition to DiseaseGenotypeHLA AntigensHumansLymphocyte ActivationReceptors, KIRRisk FactorsSarcoma, KaposiSeroepidemiologic StudiesHLA AntigensReceptors, KIRcase-control studyhuman geneticshuman leukocyte antigensItalyKaposi sarcomamajor histocompatibility complexnatural killer–cell immunoglobulin-like receptors

Identifiers

PMID26268853
PMCPMC4719589
OpenAlexW2134928781

What OpenQuestion holds

Textmetadata
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.