scholarly journals Association of MBOAT7-TMC4 rs641738 with the risk of hepatocellular carcinoma and persistent infection of hepatitis B virus: a case-control study and meta-analysis

2019 ◽  
Author(s):  
Peng Wang ◽  
Yu Zhou ◽  
Lu Li ◽  
Yajie Gong ◽  
Rong Zhong ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Case Control Study ◽  
Meta Analysis ◽  
Case Control ◽  
Hbv Infection ◽  
B Virus ◽  
Control Study

Abstract Background: Recent studies reported that a hot genetic variant, rs641738 within the membrane bound O-acyltransferase domain containing 7(MBOAT7) and transmembrane channel-like 4 (TMC4) , was associated with several liver diseases. However, results are still conflicting. We conducted this study to explore the role of MBOAT7-TMC4 rs641738 in the risk of hepatocellular carcinoma (HCC) and persistent hepatitis B virus (HBV) infection. Methods: We first performed a case-control study by including 779 HCC cases and 1412 cancer-free controls. Controls are consisted of 678 HBV persistent carriers and 734 spontaneously recovered subjects. Rs641738 was genotyped by MassARRAY platform. Results were analyzed by multivariate logistic regression analysis under five genetic models. Second, we conducted a systematic review and meta-analysis to further explore the role of this variant in HCC risk. Results: Results suggested no association between MBOAT7-TMC4 rs641738 and HCC risk in most genetic models (All P > 0.05), although a marginally significant association was observed in TT vs. CC ( P = 0.037) and recessive model ( P = 0.044). Further meta-analysis including 2135 HCC cases and 4388 controls supported that this variant was not related to HCC risk, even in the TT vs. CC and recessive models. Besides, we identified that this variant also had no influence on persistent HBV infection. Conclusion: Our work highlights that MBOAT7-TMC4 rs641738 is not associated with the risk of HCC or persistent HBV infection. This study provides some clues to identify the “truth” of potential disease-related genetic factors in the post-genome era.

scholarly journals Hepatitis B virus pre-S deletion mutations are a risk factor for hepatocellular carcinoma: a matched nested case–control study

2008 ◽  
Vol 89 (11) ◽  
pp. 2882-2890 ◽  
Author(s):  
Zhong-Liao Fang ◽  
Caroline A. Sabin ◽  
Bai-Qing Dong ◽  
Shao-Chao Wei ◽  
Qin-Yan Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Risk Factor ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Case Control Study ◽  
Case Control ◽  
Deletion Mutations ◽  
B Virus ◽  
Nested Case Control ◽  
Control Study

A matched nested case–control study of 33 paired cases and controls was conducted, based on a study cohort in Long An county, Guangxi, China, to determine whether infection with hepatitis B virus (HBV) with pre-S deletions is independently associated with the development of hepatocellular carcinoma (HCC), without the confounding effects of basal core promoter (BCP) double mutations. The prevalence of pre-S deletions was significantly higher in HCC (45.5 %, 15 of 33) than the controls (18.2 %, 6 of 33) (P<0.01), under the control of the influence of BCP double mutations. Most of the pre-S deletions occurred in, or involved, the 5′ half of the pre-S2 region and the difference between HCC (93.3 %, 14 of 15) and controls (66.7 %, four of six) was significant for this region (P=0.015). There was no significant difference in pre-S deletions between the BCP mutant group and BCP wild-type group (P>0.05), nor was the prevalence of pre-S deletions significantly different between genotypes B and C (P>0.1). These results suggest that pre-S deletions constitute an independent risk factor for HCC and their emergence and effect are independent of BCP mutations. The 5′ terminus of pre-S2 is the favoured site for the deletion mutations, especially in HCC cases. Further prospective studies are required to confirm the role of these mutations in the development of HCC.

Minor role of hepatitis B virus in the causation of chronic liver disease in Somalia indicated by a case-control study

1991 ◽  
Vol 85 (1) ◽  
pp. 104-108 ◽  
Author(s):  
Khalif Mohamud Bile ◽  
Mohamed Abdirahman ◽  
Cadigia Aden ◽  
Helene Norder ◽  
Lars Magnius ◽  
...  
Keyword(s):  
Liver Disease ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Chronic Liver Disease ◽  
Case Control Study ◽  
Case Control ◽  
Minor Role ◽  
B Virus ◽  
Control Study

scholarly journals MBOAT7-TMC4 rs641738 Is Not Associated With the Risk of Hepatocellular Carcinoma or Persistent Hepatitis B Infection

2021 ◽  
Vol 11 ◽  
Author(s):  
Peng Wang ◽  
Ying Li ◽  
Lu Li ◽  
Rong Zhong ◽  
Na Shen
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B ◽  
Meta Analysis ◽  
Hbv Infection ◽  
Genetic Models ◽  
Transmembrane Channel ◽  
B Virus ◽  
Membrane Bound ◽  
Control Study

ObjectiveA hot genetic variant, rs641738 within the membrane-bound O-acyltransferase domain containing 7(MBOAT7) and transmembrane channel-like 4 (TMC4), was recently reported to be associated with several liver diseases. However, the results remain controversial. Therefore, this study aimed to explore the role of MBOAT7-TMC4 rs641738 in the risk of hepatocellular carcinoma (HCC) and persistent hepatitis B virus (HBV) infection.MethodsWe first conducted a case-control study that included 779 HCC cases and 1412 cancer-free controls. Controls consisted of 678 persistent HBV carriers and 734 spontaneously recovered subjects. The gene variant rs641738 was genotyped using the MassARRAY platform. The results were analyzed in five genetic models using multivariate logistic regression analyses. Next, we performed a systematic review and meta-analysis to further explore the role of this variant in HCC risk.ResultsThe results suggested no association between MBOAT7-TMC4 rs641738 and HCC risk in most genetic models (all P &gt; 0.05). Although a marginally significant association was observed in TT vs. CC (P = 0.037) and the recessive models (P = 0.044). The meta-analysis of 2135 HCC cases and 4388 controls supported that this variant was not related to HCC risk, even in the TT vs. CC and recessive models. We also determined that this variant did not influence persistent HBV infection.ConclusionOur work highlights that MBOAT7-TMC4 rs641738 is not associated with the risk of HCC or persistent HBV infection. This study provides some clues to identify the “truth” of potential disease-related genetic factors in the post-genome era.

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