AI Article Synopsis
- A study investigated the connection between genetic variations in the IL12RB2 gene and lung adenocarcinoma (LAC) susceptibility.
- Researchers analyzed single nucleotide polymorphisms (SNPs) in individuals with LAC and compared them to healthy controls, finding two specific allele variants linked to a higher risk of developing the disease.
- One particular haplotype (hap18) was notably more frequent in LAC patients (18%) compared to controls (6%), suggesting that low IL-12 signaling activity may increase the likelihood of LAC development.
Article Abstract
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.
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| http://dx.doi.org/10.1016/j.imbio.2015.10.006 | DOI Listing |
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