IL12RB2 Polymorphisms correlate with risk of lung adenocarcinoma

被引：7
|
作者：
Prigione, Ignazia [1 ]
Covone, Angela Elvira [2 ]
Giacopelli, Francesca [2 ]
Bocca, Paola [1 ]
Risso, Marco [3 ]
Tripodi, Gino [3 ]
Pistorio, Angela [4 ]
Sozzi, Gabriella [5 ]
Airoldi, Irma [1 ]
Ravazzolo, Roberto [2 ,6 ]
Pistoia, Vito [1 ]
机构：
[1] Ist Giannina Gaslini, UOC Lab Oncol, I-16147 Genoa, Italy
[2] Ist Giannina Gaslini, UOC Genet Med, I-16147 Genoa, Italy
[3] Ist Giannina Gaslini, UOC Immunoematol & Med Trasfus, I-16147 Genoa, Italy
[4] Ist Giannina Gaslini, UOSD Epidemiol Biostat & Comitati, I-16147 Genoa, Italy
[5] Fdn IRCCS Ist Nazl Tumori Milano, SC Genom Tumorale, Milan, Italy
[6] Univ Genoa, Genoa, Italy
来源：
IMMUNOBIOLOGY | 2016年 / 221卷 / 02期
关键词：
Genotype-phenotype association; Lung adenocarcinoma susceptibility; STAT4; Phosphorylation; GENE POLYMORPHISMS; RECEPTOR SUBUNITS; IL-12; FAMILY; CYTOKINE; INTERLEUKIN-12; CELLS; POPULATION; ANTITUMOR; SUSCEPTIBILITY; ASSOCIATION;
D O I：
10.1016/j.imbio.2015.10.006
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
In a previous study, lack of IL-12 signaling in il12rb2 knock-out mice was found to predispose to lung adenocarcinoma (LAC). We asked whether specific polymorphisms of the human IL12RB2 gene may confer susceptibility to LAC. We studied IL12RB2 single nucleotide polymorphisms (SNPs) spanning from the promoter to the first untranslated exon of the gene. Genotypes of 49 individuals with LAC were compared with those of 93 healthy subjects. Two allele variants were found to be associated with increased susceptibility to LAC. One haplotype (hap), hap18, was more frequent in patients (18%) versus controls (6%) and significantly associated with increased probability of disease occurrence. Furthermore, IL-12 driven STAT4 phosphorylation in T cell blasts from healthy individuals was found to correlate with both single allele variants and haplotypes. In conclusion, genetically determined low signaling activity of IL-12R predisposes to the development of LAC. (C) 2015 Elsevier GmbH. All rights reserved.
引用
收藏
页码：291 / 299
页数：9
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