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ORIGINAL ARTICLE
Year : 2019  |  Volume : 32  |  Issue : 1  |  Page : 282-288

RECK gene promoter polymorphisms in patients with hepatocellular carcinoma along with chronic hepatitis C viral infection


1 Department of Clinical Pathology, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Hepatology, National Liver Institute, Menoufia University, Menoufia, Egypt
3 Department of Clinical Pathology, Ministry of Health, Bolak Al-Dakror General Hospital, Giza, Egypt

Correspondence Address:
Heba A Mostafa
Birkit El-Saba, Menoufia 32651
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_763_17

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Objective The aim was to study possible associations of reversion-inducing cysteine-rich protein with Kazal motifs (RECK) gene polymorphisms (rs11788747 and rs16932912) with the risk of developing hepatocellular carcinoma (HCC) among hepatitis C virus (HCV)-infected Egyptian patients. Background RECK is a membrane-anchored glycoprotein. Downregulation of RECK was found in a variety of neoplasms to be associated with poor survival and distant metastasis. Patients and methods The study included three groups: group I comprised 30 apparently healthy participants as a control group, group II comprised 35 patients with cirrhosis having HCV infection, and group III comprised 35 patients with cirrhosis having HCC along with HCV infection. PCR-restriction fragment length polymorphism was used for detection of RECK gene polymorphisms (rs11788747 and rs16932912). Results Regarding rs11788747, mutant AG/GG genotypes were statistically higher in HCC (60.0%) than in HCV and control groups (34.3 and 13.3%, respectively) and demonstrated 9.75 times (95% CI: 2.79–34.07) more risk of developing HCC compared with AA genotype (P < 0.001). G allele was statistically higher in HCC (51.4%) than HCV and control groups (22.9 and 8.3%, respectively). Regarding rs16932912, wild-type GG genotype was higher in HCC (71.4%) than in HCV and control groups (48.6 and 70.0%, respectively). G allele was statistically higher in HCC (81.4%) than HCV and control groups (71.4 and 83.3%, respectively) but without any statistical significance among groups regarding alleles. Conclusion RECK rs11788747 polymorphism could be involved in the pathogenesis of HCC, and rs16932912 polymorphism was not associated with the pathogenesis of HCC.


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