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Nucleotide-binding oligomerization domain-containing protein 2, encoded by , can trigger chronic gut inflammation that leads to colorectal cancer (CRC). However, studies that have investigated the association of polymorphisms and CRC susceptibility have produced inconsistent findings. To clarify this relationship, a meta-analysis was conducted to integrate data from previous studies to achieve a more precise evaluation of the risk association. PubMed, Scopus, and Web of Science databases were systematically searched to identify relevant studies on the association of polymorphisms with CRC risk. Genetic risk association was quantitatively assessed under five genetic models: homozygous, heterozygous, dominant, recessive, and allele. Thirteen studies, comprising 5,013 cases and 4,463 controls, were included in this study. Four polymorphisms were investigated in these studies, namely rs2066842, rs2066844, rs2066845, and rs2066847. Of these, only rs2066845 and rs2066847 were found to be significantly associated with increased CRC risk (rs2066845, heterozygous OR = 1.544, 95% CI = 1.014-2.349, P = 0.043; dominant OR = 1.561, 95% CI = 1.035-2.354, P = 0.034; allele OR = 1.572, 95% CI = 1.040-2.375, P = 0.032; rs2066847, heterozygous OR = 1.321, 95% CI = 1.060-1.647, P = 0.013; dominant OR = 1.402, 95% CI = 1.147-1.713, P = 0.001; allele OR = 1.345, 95% CI = 1.088-1.663, P = 0.006). In conclusion, the rs2066845 and rs2066847 polymorphisms are associated with an increased risk of CRC and may potentially serve as predisposition biomarkers for the cancer.
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http://dx.doi.org/10.3390/cancers17121999 | DOI Listing |
Cancers (Basel)
June 2025
UKM Medical Molecular Biology Institute, Universiti Kebangsaan Malaysia, Cheras 56000, Kuala Lumpur, Malaysia.
Nucleotide-binding oligomerization domain-containing protein 2, encoded by , can trigger chronic gut inflammation that leads to colorectal cancer (CRC). However, studies that have investigated the association of polymorphisms and CRC susceptibility have produced inconsistent findings. To clarify this relationship, a meta-analysis was conducted to integrate data from previous studies to achieve a more precise evaluation of the risk association.
View Article and Find Full Text PDFPLoS One
February 2023
Programa de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas, Manaus, Brazil.
Int J Mol Sci
August 2022
Department and Clinic of Hematology, Blood Neoplasms and Bone Marrow Transplantation of Wroclaw Medical University, 50-367 Wroclaw, Poland.
Toll-like receptors (TLRs), NOD-like receptors (NLRs), and RIG-I-like receptors (RLRs) are major elements of the innate immune system that recognize pathogen-associated molecular patterns. Single-nucleotide polymorphisms (SNPs) in the TLR, NLR, and RLR genes may lead to an imbalance in the production of pro- and anti-inflammatory cytokines, changes in susceptibility to infections, the development of diseases, and carcinogenesis. Acute myeloid leukemia (AML) is a bone marrow malignancy characterized by uncontrolled proliferation of transformed myeloid precursors.
View Article and Find Full Text PDFTurk J Gastroenterol
July 2021
Division of Gastroenterology, Department of Internal Medicine, Necmettin Erbakan University, Meram School of Medicine, Meram, Konya, Turkey.
Background: Hepatocellular carcinoma (HCC) is one of the important causes of mortality due to malignancy. Toll-like receptors (TLRs) are very important in liver pathophysiology in terms of their roles in the innate immune system, such as the regulation of inflammation, wound healing, stimulation of adaptive immune responses, promotion of epithelial regeneration, and carcinogenesis. In this study, we planned to examine the role of TLR1 (rs4833095, rs5743551) and nucleotide-binding oligomerization domain (NOD2) (rs2066844, rs2066845, rs2066847) polymorphisms in the development of HCC and their effects on the clinical presentation of HCC patients.
View Article and Find Full Text PDFGenes (Basel)
June 2021
Department of Gastroenterology and Hepatology, University Hospital Heidelberg, INF 410, 69120 Heidelberg, Germany.