Alcoholic Cirrhosis and Hepatocellular Carcinoma

Stickel, Felix

doi:10.1007/978-3-319-09614-8_7

Cited by 42 publications

(26 citation statements)

References 86 publications

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“…1). 18 A great concern is the rising incidence of hepatocellular carcinoma (HCC) which evolves in approximately 1% to 2% of alcoholic cirrhotics per year 19. While steatosis and inflammation are reversible upon abstinence, and probably also fibrosis below the level of cirrhotic transformation, severe alcoholic steatohepatitis (ASH), decompensating cirrhosis and HCC have a grave prognosis.…”

Section: Spectrum and Pathophysiology Of Aldmentioning

confidence: 99%

Pathophysiology and Management of Alcoholic Liver Disease: Update 2016

et al. 2017

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Alcoholic liver disease (ALD) is a leading cause of cirrhosis, liver cancer, and acute and chronic liver failure and as such causes significant morbidity and mortality. While alcohol consumption is slightly decreasing in several European countries, it is rising in others and remains high in many countries around the world. The pathophysiology of ALD is still incompletely understood but relates largely to the direct toxic effects of alcohol and its main intermediate, acetaldehyde. Recently, novel putative mechanisms have been identified in systematic scans covering the entire human genome and raise new hypotheses on previously unknown pathways. The latter also identify host genetic risk factors for significant liver injury, which may help design prognostic risk scores. The diagnosis of ALD is relatively easy with a panel of well-evaluated tests and only rarely requires a liver biopsy. Treatment of ALD is difficult and grounded in abstinence as the pivotal therapeutic goal; once cirrhosis is established, treatment largely resembles that of other etiologies of advanced liver damage. Liver transplantation is a sound option for carefully selected patients with cirrhosis and alcoholic hepatitis because relapse rates are low and prognosis is comparable to other etiologies. Still, many countries are restrictive in allocating donor livers for ALD patients. Overall, few therapeutic options exist for severe ALD. However, there is good evidence of benefit for only corticosteroids in severe alcoholic hepatitis, while most other efforts are of limited efficacy. Considering the immense burden of ALD worldwide, efforts of medical professionals and industry partners to develop targeted therapies in ALF has been disappointingly low.

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Section: Spectrum and Pathophysiology Of Aldmentioning

confidence: 99%

Pathophysiology and Management of Alcoholic Liver Disease: Update 2016

et al. 2017

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“…The mechanisms by which NASH and ASH progress to HCC are not completely understood and the re are many theories including chromosomal loss of tumor suppressor genes, oxidative stress, decreased liver retinoic acid level, altered DNA methylation, and genetic susceptibility [Morgan et al, 2004][Stickel et al, 2002, 2015]. In our previous studies, we showed that in addition to the TLR/NFKB/CXCR4/7 [Liu et al, 2014][French et al, 2012][Nan et al, 2005][French et al, 2010] and PI3K/AKT/mTORC1 signaling pathways [Afifiyan et al, 2017], Tec kinase signaling pathway connects these two systems together in Mallory-Denk Bodies (MDB) formation both in ASH and NASH [Afifiyan et al, 2017].…”

Section: Introductionmentioning

confidence: 99%

Different roles of FAT10, FOXO1, and ADRA2A in hepatocellular carcinoma tumorigenesis in patients with alcoholic steatohepatitis (ASH) vs non-alcoholic steatohepatitis (NASH)

Jia

French

Tillman

et al. 2018

Experimental and Molecular Pathology

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Hepatocellular carcinoma (HCC) is the fifth most common cancer and the second leading cause of cancer related deaths worldwide. Among others, non-alcoholic steatohepatitis (NASH) and alcoholic steatohepatitis (ASH) are the two major risk factors as both of them may develop cirrhosis and hepatocellular carcinoma (HCC) if left untreated. However, patients with NASH progress to HCC at a rate around 0.5% annually, while 3–10% ASH patients may progress to HCC annually. The present study is to demonstrate the molecular differences in oncogenesis pathway between NASH and ASH. By using immunofluorescence study and quantitating the fluorescence intensity morphometrically in liver biopsied specimens from NASH and ASH patients, the protein expression of candidate molecules within hepatocytes cytoplasm are studied, including two HCC-related molecules FAT10 and FOXO1, and one GPCR pathway related molecule ADRA2A. Compared with the control group patients, the expression levels of all the molecules were upregulated in the ASH group of patients(p<0.001 in all molecules), while FAT10 and ADRA2A were upregulated, FOXO1 did not change in the NASH group of patients.The most important finding is that compared with the ASH group of patients, the expression levels of all three molecules were significantly lower than in the NASH group of patients (p<0.001 in all molecules). These results confirmed our previous finding that there are significant differences of molecules change in ASH compared to NASH. Thus, we conclude that there are significantly different molecules and pathways involved during the pathogenesis of HCC development in ASH compared to NASH which could help explain why the tumorigenic rate is different in ASH and NASH.

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“…More than 80% of reported HCC cases occur in the Eastern and Southern Asia and in the sub-Saharan Africa, where its incidence is greater than 20 patients per 100,000 individuals (2) and is mainly associated with epidemic chronic HBV infection and aflatoxin B 1 (AFB1) exposure (1,3). In contrast, the prevalence of HCC cases in the United States and Europe is mainly associated with a chronic HCV infection, chronic alcohol consumption, and NAFLD (1,4,5).…”

Section: Introductionmentioning

confidence: 85%

Nutritional Epigenetics and the Prevention of Hepatocellular Carcinoma with Bioactive Food Constituents

Moreno

Heidor

Pogribny

2016

Nutrition and Cancer

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Hepatocellular carcinoma (HCC) is an aggressive and life-threatening disease often diagnosed at intermediate or advanced stages, which substantially limits therapeutic approaches to its successful treatment. This indicates that the prevention of HCC may be the most promising strategy in reducing its incidence and mortality. Emerging evidence indicates that numerous nutrients and nonnutrient dietary bioactive components can reduce the occurrence and/or delay the development of HCC through modifications of deregulated epigenetic mechanisms. This review examines the existing knowledge on the epigenetic mechanism-based studies in in vitro and in vivo models of HCC on the chemopreventive potential of epigenetic food components, including dietary methyl-group donors, epigallocatechin-3-gallate, sodium butyrate, resveratrol, curcumin, and sulforaphane, on liver carcinogenesis. Future direction and potential challenges in the effective use of bioactive food constituents in the prevention of HCC are highlighted and discussed.

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Alcoholic Cirrhosis and Hepatocellular Carcinoma

Cited by 42 publications

References 86 publications

Pathophysiology and Management of Alcoholic Liver Disease: Update 2016

Pathophysiology and Management of Alcoholic Liver Disease: Update 2016

Different roles of FAT10, FOXO1, and ADRA2A in hepatocellular carcinoma tumorigenesis in patients with alcoholic steatohepatitis (ASH) vs non-alcoholic steatohepatitis (NASH)

Nutritional Epigenetics and the Prevention of Hepatocellular Carcinoma with Bioactive Food Constituents

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