NOD2/CARD15 polymorphisms impair innate immunity and increase susceptibility to gastric cancer in an Italian population

Angeletti, Silvia; Galluzzo, Sara; Santini, Daniele; Ruzzo, Annamaria; Vincenzi, Bruno; Ferraro, Elisabetta; Spoto, Chiara; Lorino, G.; Graziano, N.; Calvieri, Alice; Magnani, Mauro; Graziano, Francesco; Pantano, Francesco; Tonini, Giuseppe; Dicuonzo, Giordano

doi:10.1016/j.humimm.2009.04.026

Cited by 30 publications

(24 citation statements)

References 29 publications

(32 reference statements)

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“…ACS ϭ acute coronary syndrome; CAD ϭ coronary artery disease. gastric cancer [19]. The role of both vascular inflammation and the immune system in the pathogenesis of atherosclerosis is well known [1]; however, to date no study has evaluated the impact of NOD2/CARD15 gene polymorphisms on coronary atherosclerosis documented by coronary angiography.…”

Section: Discussionmentioning

confidence: 99%

Association between NOD2/CARD15 polymorphisms and coronary artery disease: a case–control study

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Association between NOD2/CARD15 polymorphisms and coronary artery disease: a case–control study

et al. 2011

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“…Studies, conducted in a number of populations, have investigated the association between the polymorphisms NOD1 rs2907749 (246), NOD1 rs7789045 (246), NOD1 rs2075820 (E266K) (179, 247), NOD1 rs5743336 (180), NOD2 rs7205423 (246), NOD2 rs7202124 (164), NOD2 rs2111235 (164), NOD2 rs5743289 (164), NOD2 rs2066842 (P268S) (248, 249), NOD2 rs2066844 (R702W) (250), NOD2 rs2066845 (G908R) (184), and NOD2 rs2066847 (L1007insC) (184, 250), and risk of gastric precancerous lesions and GC (Table 3). Further, a recent meta-analysis by Liu et al (251) that included six case–control studies has shown consistent associations between NOD2 R702W, G908R, and L1007insC, and risk of GC.…”

Section: Nod-like Receptors and Helicobacter Pylori-related Gastric Cmentioning

confidence: 99%

Pattern-Recognition Receptors and Gastric Cancer

2014

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Chronic inflammation has been associated with an increased risk of several human malignancies, a classic example being gastric adenocarcinoma (GC). Development of GC is known to result from infection of the gastric mucosa by Helicobacter pylori, which initially induces acute inflammation and, in a subset of patients, progresses over time to chronic inflammation, gastric atrophy, intestinal metaplasia, dysplasia, and finally intestinal-type GC. Germ-line encoded receptors known as pattern-recognition receptors (PRRs) are critical for generating mature pro-inflammatory cytokines that are crucial for both Th1 and Th2 responses. Given that H. pylori is initially targeted by PRRs, it is conceivable that dysfunction within genes of this arm of the immune system could modulate the host response against H. pylori infection, and subsequently influence the emergence of GC. Current evidence suggests that Toll-like receptors (TLRs) (TLR2, TLR3, TLR4, TLR5, and TLR9), nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) (NOD1, NOD2, and NLRP3), a C-type lectin receptor (DC-SIGN), and retinoic acid-inducible gene (RIG)-I-like receptors (RIG-I and MDA-5), are involved in both the recognition of H. pylori and gastric carcinogenesis. In addition, polymorphisms in genes involved in the TLR (TLR1, TLR2, TLR4, TLR5, TLR9, and CD14) and NLR (NOD1, NOD2, NLRP3, NLRP12, NLRX1, CASP1, ASC, and CARD8) signaling pathways have been shown to modulate the risk of H. pylori infection, gastric precancerous lesions, and/or GC. Further, the modulation of PRRs has been suggested to suppress H. pylori-induced inflammation and enhance GC cell apoptosis, highlighting their potential relevance in GC therapeutics. In this review, we present current advances in our understanding of the role of the TLR and NLR signaling pathways in the pathogenesis of GC, address the involvement of other recently identified PRRs in GC, and discuss the potential implications of PRRs in GC immunotherapy.

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“…Owing to its role in the regulation of the immune response, apoptosis, cell cycle, and other cell division mechanisms, the NF-κB activity was found to be significantly elevated in several human malignancies, e.g., thyroid, breast, lung, and colorectal cancers (Gilmore et al, 1996;Chen et al, 2001). In fact, NOD2/CARD15 variants were also associated with the development of several human malignancies, i.e., gastric and breast cancers, as well as nonHodgkin's lymphoma (Huzarski et al, 2005;Rothman et al, 2006;Angeletti et al, 2009). …”

Section: Discussionmentioning

confidence: 99%

NOD2/CARD15 variants in Malaysian patients with sporadic colorectal cancer

Lau¹,

Roslani²,

Lian³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Colorectal cancer (CRC) is one of the most common types of cancer in both developed and developing countries. This disease is triggered by and progresses via the sequential accumulation of multiple genetic alterations. In addition, the interaction between lowpenetrance genes and environmental factors can also increase the risk of developing CRC. Since inflammatory bowel diseases (IBDs) are one of the predisposing factors for CRC, IBD-related genes might, to a certain extent, be associated with cancer initiation. The nucleotide oligomerization domain 2/caspase activating recruitment domain 15 gene (NOD2/CARD15) is the most well-established gene to be associated with increased susceptibility to Crohn's disease. Thus, various studies have been performed to investigate the potential contribution of this gene to CRC risk. In this study, we aimed to determine the frequency of the Arg702Trp, Gly908Arg, 3020insC, Pro268Ser, and JW1 variants of NOD2/CARD15, and to investigate their association with CRC susceptibility. A total of 130 CRC patients and 212 healthy controls were recruited for this study. Subsequently, real-time polymerase chain reaction with TaqMan was performed for the genotyping of these NOD2/ CARD15 variants. None of the NOD2/CARD15 variants was statistically associated to CRC susceptibility in our Malaysian population. Our findings were remarkably similar to those of other Asian cohorts, which indicated that these NOD2/CARD15 variants exhibit genetic heterogeneity between Caucasian and Asian populations.

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NOD2/CARD15 polymorphisms impair innate immunity and increase susceptibility to gastric cancer in an Italian population

Cited by 30 publications

References 29 publications

Association between NOD2/CARD15 polymorphisms and coronary artery disease: a case–control study

Association between NOD2/CARD15 polymorphisms and coronary artery disease: a case–control study

Pattern-Recognition Receptors and Gastric Cancer

NOD2/CARD15 variants in Malaysian patients with sporadic colorectal cancer

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