Genetics and Genomics of Liver Disease

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (20 March 2021) | Viewed by 4816

Special Issue Editor


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Guest Editor
Saga University Hospital, Faculty of Medicine, Saga University, 5-1-1, Nabeshima, Saga, Japan
Interests: metabolic syndrome; nonalcoholic steatohepatitis; diabetes; translational research; RNAseq; mRNA array; GWAS

Special Issue Information

Dear Colleagues,

Genetics and genomics influence the pathogenesis and outcome of liver disease, including viral hepatitis, alcoholic liver injury, nonalcoholic steatohepatitis, and autoimmune liver diseases. The recent development of the genome-wide approach, exome and whole-genome sequencing, and sequencing-based studies of gene expression have accelerated genetics and genomics research. Single nucleotide polymorphism is associated with the disease phenotype, treatment effect, and prognosis. Therefore, tailor-made strategies are utilized for more effective prevention and treatment, along with the recent pharmacological development, changing the treatment strategy and outcome of liver diseases. Sequencing-based studies and omics identify the therapeutic target of chronic liver disease and contribute to the development of biomarkers. This Special Issue widely calls for research involving human subjects and model organisms that investigate the impact of genetics and genomics on liver disease.

Dr. Hirokazu Takahashi
Guest Editor

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Keywords

  • viral hepatitis
  • liver diseases
  • hepatocellular carcinoma
  • SNP
  • gene variant
  • RNA expression
  • genome-wide
  • fatty liver

Published Papers (2 papers)

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Research

15 pages, 1713 KiB  
Article
High SGO2 Expression Predicts Poor Overall Survival: A Potential Therapeutic Target for Hepatocellular Carcinoma
by Min Deng, Shaohua Li, Jie Mei, Wenping Lin, Jingwen Zou, Wei Wei and Rongping Guo
Genes 2021, 12(6), 876; https://doi.org/10.3390/genes12060876 - 7 Jun 2021
Cited by 3 | Viewed by 2267
Abstract
Shugoshin2 (SGO2) may participate in the occurrence and development of tumors by regulating abnormal cell cycle division, but its prognostic value in hepatocellular carcinoma (HCC) remains unclear. In this study, we accessed The Cancer Genome Atlas (TCGA) database to get the clinical data [...] Read more.
Shugoshin2 (SGO2) may participate in the occurrence and development of tumors by regulating abnormal cell cycle division, but its prognostic value in hepatocellular carcinoma (HCC) remains unclear. In this study, we accessed The Cancer Genome Atlas (TCGA) database to get the clinical data and gene expression profile of HCC. The expression of SGO2 in HCC tissues and nontumor tissues and the relationship between SGO2 expression, survival, and clinicopathological parameters were analyzed. The SGO2 expression level was significantly higher in HCC tissues than in nontumor tissues (p < 0.001). An analysis from the Oncomine and Gene Expression Profiling Interactive Analysis 2 (GEPIA2) databases also demonstrated that SGO2 was upregulated in HCC (all p < 0.001). A logistic regression analysis revealed that the high expression of SGO2 was significantly correlated with gender, tumor grade, pathological stage, T classification, and Eastern Cancer Oncology Group (ECOG) score (all p < 0.05). The overall survival (OS) of HCC patients with higher SGO2 expression was significantly poor (p < 0.001). A multivariate analysis showed that age and high expression of SGO2 were independent predictors of poor overall survival (all p < 0.05). Twelve signaling pathways were significantly enriched in samples with the high-SGO2 expression phenotype. Ten proteins and 34 genes were significantly correlated with SGO2. In conclusion, the expression of SGO2 is closely related to the survival of HCC. It may be used as a potential therapeutic target and prognostic marker of HCC. Full article
(This article belongs to the Special Issue Genetics and Genomics of Liver Disease)
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12 pages, 4776 KiB  
Article
The Effect of Genetic Polymorphism in Response to Body Weight Reduction in Japanese Patients with Nonalcoholic Fatty Liver Disease
by Yuya Seko, Kanji Yamaguchi, Nozomi Tochiki, Kota Yano, Aya Takahashi, Shinya Okishio, Seita Kataoka, Keiichiroh Okuda, Atsushi Umemura, Michihisa Moriguchi and Yoshito Itoh
Genes 2021, 12(5), 628; https://doi.org/10.3390/genes12050628 - 22 Apr 2021
Cited by 10 | Viewed by 1882
Abstract
Background: weight loss as a result of lifestyle intervention is effective when treating non-alcoholic fatty liver disease (NAFLD). We estimated the effects of PNPLA3 rs738409 and HSD17B13 rs6834314 variants in response to diet therapy in Japanese patients with NAFLD. Methods: we analyzed the [...] Read more.
Background: weight loss as a result of lifestyle intervention is effective when treating non-alcoholic fatty liver disease (NAFLD). We estimated the effects of PNPLA3 rs738409 and HSD17B13 rs6834314 variants in response to diet therapy in Japanese patients with NAFLD. Methods: we analyzed the correlation between the change in liver stiffness and change in body weight in 140 patients administered diet therapy for 1-year, according to PNPLA3 and HSD17B13 genotypes. Results: the bodyweight (BW) reduction rate was greater in patients with the PNPLA3 genotype CC than CG and GG (p = 0.035). Change in liver stiffness measurement (LSM) was significantly associated with a change in BW in PNPLA3 CG/GG (r = 0.279/0.381), but not in PNPLA3 CC (p = 0.187). Change in LSM was correlated with change in BW only in patients with HSD17B13 AG/GG (r = 0.425), but not the AA genotype (p = 0.069). A multivariate analysis identified that a change in LSM was correlated with a change in BW in carriers of HSD17B13 AG/GG (B = 3.043, p = 0.032), but not HSD17B13 AA. The change in LSM of patients with a BW reduction of more than 7% (0.50) was significantly greater than that of patients with a BW reduction of less than 7% (0.83) (p = 0.038). Conclusions: in Japanese patients with NAFLD, HSD17B13 rs6834314 polymorphism is associated with the change in LSM by lifestyle intervention. The approach, including genetic assessments, may contribute to the establishment of appropriate therapeutic strategies to treat NAFLD. Full article
(This article belongs to the Special Issue Genetics and Genomics of Liver Disease)
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