Genome-wide association pathway analysis to identify candidate single nucleotide polymorphisms and molecular pathways associated with TP53 expression status in HBV-related hepatocellular carcinoma

Liao, Xiwen; Liu, Yu; Liu, Xiaoguang; Han, Chuangye; Yu, Tingdong; Yang, Chengkun; Zhu, Guangzhi; Su, Hao; Peng, Tao

doi:10.2147/cmar.s163209

Cited by 11 publications

(8 citation statements)

References 53 publications

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“…Of the 12 SNPs reported in HBV-related HCC GWASs, rs2647073 and rs3997872 near HLA-DRB1 were found to be significantly associated with the risk of HBV-related LC, which suggested that genetic variants associated with HBV-related hepatocarcinogenesis may already play an important role in the progression from CHB to LC [43]. A recent study reported new SNPs at HLA-DRB 1 (rs35445101) associated with TP53 expression status in HBV-related hepatocellular carcinoma [30].…”

Section: Hla Class II Allele Polymorphism and Hbv Infection Outcomesmentioning

confidence: 99%

“…Chang et al found that rs9276370 (HLA-DQA 2 ), rs7756516, and rs7453920 (HLA-DQB 2 ) are significantly associated with persistent HBV infection, especially the "T-T" haplotype composed of rs7756516 and rs9276370 that is more prevalent in severe disease subgroups and associated with nonsustained therapeutic response in male Taiwan Han Chinese individuals [49]. A nearest study reported four new SNPs at HLA-DQB 1 (rs1130399, rs1049056, rs1049059, and rs1049060) associated with TP53 expression status in HBV-related HCC [30].…”

Section: Hla Class II Allele Polymorphism and Hbv Infection Outcomesmentioning

confidence: 99%

“…Han Chinese individuals [49]. A nearest study reported a new SNP at HLA-DPB1 (rs1042153) associated with TP53 expression status in HBV-related hepatocellular carcinoma [30].…”

Section: Hla Class II Allele Polymorphism and Hbv Infection Outcomesmentioning

confidence: 99%

“…Since 1979, Kew et al [25] started the research for the association between histocompatibility antigens and HBV infection, and a plenty of researches demonstrated that the highly polymorphic HLA classes I and II genes can affect the ability of HLA molecules to trigger immune responses, which affects the outcomes of HBV infection, and discrepant conclusions were reached in different cohorts [26,27]. HLA class II gene polymorphisms are strongly associated with not only persistent HBV infection but also spontaneous HBV clearance and seroconversion, disease progression, and the development of LC and HBV-related HCC in chronic hepatitis B [28][29][30]. This chapter summarizes the reported associations of HLA class II gene polymorphisms with susceptibility to HBV infection, resolution, and disease progression and their related mechanisms.…”

Section: Introductionmentioning

confidence: 99%

“…gene variations are strongly associated with HBV infection outcomes in not only HLA alleles but also single nucleotide polymorphisms (SNPs) identified through genome-wide associated studies (GWASs). Recent GWASs have revealed several SNPs at HLA class II region associated with the risk of HBV infection[23,30].A Chinese study by Zhu et al[40] identified two HLA-DR loci that independently drive chronic HBV infection, including HLA-DRβ113 sites 71 and rs400488. Acute-on-chronic liver failure (ACLF) is an extreme condition after severe acute exacerbation of chronic hepatitis B. Tan et al carried out a genome-wide association study, among 1300 ACLFs and 2087 AsCs, and identified rs3129859 at HLA class II region (chromosome 6p21.32) which is associated with HBV-related ACLF.…”

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confidence: 99%

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HLA Class II Allele Polymorphisms and the Clinical Outcomes of HBV Infection

Zhang¹

2019

Human Leukocyte Antigen (HLA)

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In 2016, the global health sector strategy (GHSS) on viral hepatitis called for elimination of hepatitis B as a major public health threat by 2030 (i.e., 90% reduction in incidence and 65% in mortality). But persistence or clearance of hepatitis B virus (HBV) infection mainly depends upon host immune responses. The human leukocyte antigen (HLA) system is the center of host immune responses. HLA genes are located in chromosome 6p21.31 and cover 0.13% of the human genome and show a high degree of polymorphism and extensive patterns of linkage disequilibrium (LD), which differ among populations. The HLA genes include HLA class I, HLA class II, and other non-HLA alleles. HLA class II gene polymorphisms are strongly associated with not only persistent HBV infection but also spontaneous HBV clearance and seroconversion, disease progression, and the development of liver cirrhosis (LC) and HBV-related hepatocellular carcinoma (HCC) in chronic hepatitis B. This chapter summarizes the reported associations of HLA class II gene polymorphisms with the outcomes of HBV infection and their related mechanisms.

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Section: Hla Class II Allele Polymorphism and Hbv Infection Outcomesmentioning

confidence: 99%

Section: Hla Class II Allele Polymorphism and Hbv Infection Outcomesmentioning

confidence: 99%

“…Han Chinese individuals [49]. A nearest study reported a new SNP at HLA-DPB1 (rs1042153) associated with TP53 expression status in HBV-related hepatocellular carcinoma [30].…”

Section: Hla Class II Allele Polymorphism and Hbv Infection Outcomesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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HLA Class II Allele Polymorphisms and the Clinical Outcomes of HBV Infection

Zhang¹

2019

Human Leukocyte Antigen (HLA)

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Genetic variants of the peroxisome proliferator‐activated receptor (PPAR) signaling pathway genes and risk of pancreatic cancer

Liu

Qian

Liu

et al. 2020

Molecular Carcinogenesis

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Because the peroxisome proliferator‐activated receptor (PPAR) signaling pathway is involved in development and progression of pancreatic cancer, we investigated associations between genetic variants of the PPAR pathway genes and pancreatic cancer risk by using three published genome‐wide association study datasets including 8477 cases and 6946 controls of European ancestry. Expression quantitative trait loci (eQTL) analysis was also performed for correlations between genotypes of the identified genetic variants and messenger RNA (mRNA) expression levels of their genes by using available databases of the 1000 Genomes, TCGA, and GTEx projects. In the single‐locus logistic regression analysis, we identified 1141 out of 17 532 significant single‐nucleotide polymorphisms (SNPs) in 112 PPAR pathway genes. Further multivariate logistic regression analysis identified three independent, potentially functional loci (rs12947620 in MED1, rs11079651 in PRKCA, and rs34367566 in PRKCB) for pancreatic cancer risk (odds ratio [OR] = 1.11, 95% confidence interval [CI], [1.06‐1.17], P = 5.46 × 10−5; OR = 1.10, 95% CI, [1.04‐1.15], P = 1.99 × 10−4; and OR = 1.09, 95% CI, [1.04‐1.14], P = 3.16 × 10−4, respectively) among 65 SNPs that passed multiple comparison correction by false discovery rate (< 0.2). When risk genotypes of these three SNPs were combined, carriers with 2 to 3 unfavorable genotypes (NUGs) had a higher risk of pancreatic cancer than those with 0 to 1 NUGs. The eQTL analysis showed that rs34367566 A>AG was associated with decreased expression levels of PRKCB mRNA in 373 lymphoblastoid cell lines. Our findings indicate that genetic variants of the PPAR pathway genes, particularly MED1, PRKCA, and PRKCB, may contribute to susceptibility to pancreatic cancer.

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