Are Pattern Recognition Receptors Associated with Hepatocellular Carcinoma?
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Abstract
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.
Methods: Our study was designed prospectively. Cirrhotic and HCC patients who were followed up in our clinic between January 2015 and
September 2018 were included in the study. Sex, age, cirrhosis etiology, Child–Pugh class, and MELD scores were recorded. TLR1 and
NOD2 polymorphisms were studied by the PCR method.
Results: HCC developed in 88 (31.4%) of the 280 patients who were followed up, either during the recruitment phase of our study
or during the follow-up. The mean follow-up time of our patient group was 17.04 ± 11.72 months, and the mean follow-up time of
HCC patients was 12.09 ± 10.26 months. TLR1 (rs5743551) polymorphism was associated with HCC development (P = .003). TLR1
(rs5743551) and NOD2 (rs2066844) polymorphisms were associated with the development of spontaneous bacterial peritonitis (SBP)
in the HCC patient group (P = .013 and P = .021, respectively).
Conclusion: We think that increased bacterial translocation in cirrhotic patients may contribute to HCC development by causing chronic
inflammation, especially in patients with TLR 1 (rs5743551) polymorphism.
(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.
Methods: Our study was designed prospectively. Cirrhotic and HCC patients who were followed up in our clinic between January 2015 and
September 2018 were included in the study. Sex, age, cirrhosis etiology, Child–Pugh class, and MELD scores were recorded. TLR1 and
NOD2 polymorphisms were studied by the PCR method.
Results: HCC developed in 88 (31.4%) of the 280 patients who were followed up, either during the recruitment phase of our study
or during the follow-up. The mean follow-up time of our patient group was 17.04 ± 11.72 months, and the mean follow-up time of
HCC patients was 12.09 ± 10.26 months. TLR1 (rs5743551) polymorphism was associated with HCC development (P = .003). TLR1
(rs5743551) and NOD2 (rs2066844) polymorphisms were associated with the development of spontaneous bacterial peritonitis (SBP)
in the HCC patient group (P = .013 and P = .021, respectively).
Conclusion: We think that increased bacterial translocation in cirrhotic patients may contribute to HCC development by causing chronic
inflammation, especially in patients with TLR 1 (rs5743551) polymorphism.