Copy number gain of pro-inflammatory genes in patients with HBV-related acute-on-chronic liver failure

Sun, Fengming; Tan, Wenting; Dan, Yunjie; Wang, Xiuhua; Guo, Yanzhi; Deng, Guohong

doi:10.1186/s12920-020-00835-5

Cited by 3 publications

(2 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…through immune response. The genetic susceptibility and copy number variations were critical for severe hepatitis B flare and have an important role in the pathogenesis of HBV-related ACLF [ 37 – 39 ]. However, one of the limitations of our study is that we did not take into account host genetic factors.…”

Section: Discussionmentioning

confidence: 99%

A Lower HCC Incidence in Chronic HBV-Infected Patients Recovered from Acute-on-Chronic Liver Failure: A Prospective Cohort Study

Yin

et al. 2022

Journal of Oncology

View full text Add to dashboard Cite

Background. Activation of chronic hepatitis B virus (HBV) infection is an important cause of acute-on-chronic liver failure (ACLF). However, the effect of HBV-ACLF episode on hepatocellular carcinoma (HCC) occurrence remains largely unknown. Methods. A total of 769 HBV-ACLF patients and 2114 HBV-related chronic liver disease (HBV-CLD) patients diagnosed between August 1998 and December 2011 were enrolled in this prospective cohort study. Of the HBV-CLD patients, 380 received lifetime antiviral treatment with nucleos(t)ide analogues. Propensity score matching was applied to reduce baseline differences between HBV-ACLF and HBV-CLD cohorts. Results. The survival rate of HBV-ACLF patients was 53.6%, 50.3%, 47.8%, and 46.2% at 90-day, 1-year, 5-year, and 10-year, respectively. The cumulative incidence of HCC was lower in HBV-ACLF cohort with 369 eligible patients survived for >90 days than in HBV-CLD cohort with the 380 patients (5.77/1,000 vs. 9.78/1,000 person-years, p = 0.0497 ). HBV-ACLF episode decreased HCC risk regardless of liver cirrhosis, and in patients without family history of HCC. Multivariate Cox analyses indicated that male, increasing age, liver cirrhosis, and platelet count (≤100 × 109/L) increased, whereas HBV-ACLF episode decreased, HCC risk independently. In the propensity score-matched cohorts, HBV-ACLF episode reduced HCC incidence (10.20/1,000 vs. 4.66/1,000 person-years, p = 0.0326 ). The area under curve of nomogram was 0.812 for 3-year HCC probability. Conclusions. HBV-ACLF episode decreases HCC occurrence in chronic HBV patients. Older age and liver cirrhosis independently increased HCC occurrence. A nomogram-enrolled episode of ACLF reliably predicts the occurrence of HCC.

show abstract

Section: Discussionmentioning

confidence: 99%

A Lower HCC Incidence in Chronic HBV-Infected Patients Recovered from Acute-on-Chronic Liver Failure: A Prospective Cohort Study

Yin

et al. 2022

Journal of Oncology

View full text Add to dashboard Cite

show abstract

“…In particular, CNV genotyping was crucial in studies involving diseases such as schizophrenia [ 216 , 217 ], bipolar disorder [ 216 ], Parkinson’s disease [ 218 ], Autism Spectrum Disorder [ 219 ] and attention deficit hyperactivity disorder [ 220 ]. Other CNVs studies included different outcomes such as HBV [ 221 , 222 ], autophagy [ 223 ], gallstones disease [ 224 ], vesicoureteral reflux [ 225 ], esotropia [ 226 ], cheap screenings for primary immunodeficiency [ 227 ] and COVID-19 potential targets [ 228 ]. For these studies, PennCNV was the most popular, followed by Nexus Copy Number, Birdsuite and QuantiSNP.…”

Section: Recent Studies Applying Inference Methods Of Snp Datamentioning

confidence: 99%

Fully exploiting SNP arrays: a systematic review on the tools to extract underlying genomic structure

Balagué-Dobón

Cáceres

González

2022

Briefings in Bioinformatics

View full text Add to dashboard Cite

Single nucleotide polymorphisms (SNPs) are the most abundant type of genomic variation and the most accessible to genotype in large cohorts. However, they individually explain a small proportion of phenotypic differences between individuals. Ancestry, collective SNP effects, structural variants, somatic mutations or even differences in historic recombination can potentially explain a high percentage of genomic divergence. These genetic differences can be infrequent or laborious to characterize; however, many of them leave distinctive marks on the SNPs across the genome allowing their study in large population samples. Consequently, several methods have been developed over the last decade to detect and analyze different genomic structures using SNP arrays, to complement genome-wide association studies and determine the contribution of these structures to explain the phenotypic differences between individuals. We present an up-to-date collection of available bioinformatics tools that can be used to extract relevant genomic information from SNP array data including population structure and ancestry; polygenic risk scores; identity-by-descent fragments; linkage disequilibrium; heritability and structural variants such as inversions, copy number variants, genetic mosaicisms and recombination histories. From a systematic review of recently published applications of the methods, we describe the main characteristics of R packages, command-line tools and desktop applications, both free and commercial, to help make the most of a large amount of publicly available SNP data.

show abstract

Interleukin-18 Plays a Positive Feedback Activity to Natural Killer-Like B Cells in Hepatitis B Virus-Associated Acute-on-Chronic Liver Failure

Liu¹,

Xing²,

Wang³

et al. 2022

Viral Immunology

View full text Add to dashboard Cite

Copy number gain of pro-inflammatory genes in patients with HBV-related acute-on-chronic liver failure

Cited by 3 publications

References 40 publications

A Lower HCC Incidence in Chronic HBV-Infected Patients Recovered from Acute-on-Chronic Liver Failure: A Prospective Cohort Study

A Lower HCC Incidence in Chronic HBV-Infected Patients Recovered from Acute-on-Chronic Liver Failure: A Prospective Cohort Study

Fully exploiting SNP arrays: a systematic review on the tools to extract underlying genomic structure

Interleukin-18 Plays a Positive Feedback Activity to Natural Killer-Like B Cells in Hepatitis B Virus-Associated Acute-on-Chronic Liver Failure

Contact Info

Product

Resources

About