Molecular Pathogenesis of Hepatocellular Carcinoma

McKillop, Iain H.; Moran, Diarmuid M.; Jin, Xiaodong; Koniaris, Leonidas G.

doi:10.1016/j.jss.2006.04.013

Cited by 95 publications

(104 citation statements)

References 104 publications

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“…HBV or HCV chronic infection is the most overwhelming environmental factor for HCC susceptibility globally, especially in developing countries (McKillop et al, 2006). Theoretically, HBV/HVC carriers would be more susceptible to HCC.…”

Section: Discussionmentioning

confidence: 99%

“…Genome integrity and DNA damages have shed light on the mechanisms that concealed in HCC development (Price et al, 2013). Hepatitis B virus is the most common environmental cause of HCC susceptibility (>80%) which usually leads to DNA damages (McKillop et al, 2006). In addition, aflatoxin B1, alcohol consumption and cigarette smoking (Akinyinka et al, 2001;Lopez et al, 2004) also contribute pivotally to HCC occurrence due to unrepaired DNA damages (Stem et al, 2002;Lahtz et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

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The XRCC1 Arg399Gln Genetic Polymorphism Contributes to Hepatocellular Carcinoma Susceptibility: An Updated Meta-analysis

Pan¹,

Zhao²,

Chen³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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The potential correlation of X-ray repair cross-complementing group 1 (XRCC1) Arg399Gln polymorphism with hepatocellular carcinoma (HCC) susceptibility is ambiguous. Taking account of inconsistent results of previous meta-analyses and new emerging literatures, we conducted a meta-analysis covering 15 case-control datasets to evaluate the relationship. Relevant studies from Medline, Embase and CNKI were retrieved. A fixedeffect model or a random-effect model, depending on between-study heterogeneity, were applied to estimate the association between XRCC1 polymorphism Arg399Gln and HCC risk with the results presented as odds ratios (ORs) and 95% confidence intervals (95% CIs). In accordance with Hardy-Weinberg equilibrium, 15 studies with data for 6,556 individuals were enrolled in this systematic review.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The XRCC1 Arg399Gln Genetic Polymorphism Contributes to Hepatocellular Carcinoma Susceptibility: An Updated Meta-analysis

Pan¹,

Zhao²,

Chen³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…3 To circumvent this problem, a number of innovative therapies have been used, including portal vein embolization and staged liver resections, although both can be associated with considerable morbidity and mortality. [4][5][6] Little work has examined the mechanisms of liver failure after extreme liver resection. The current literature suggests that failure of liver regeneration in such settings is attributable to excessive hepatocyte apoptosis.…”

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confidence: 99%

Interleukin-6 inhibits oxidative injury and necrosis after extreme liver resection

et al. 2007

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Extreme hepatectomy or resection of more than 80% of liver mass often leads to liver failure and death and is a major limitation to therapeutic liver resection for patients with liver tumors. We sought to define the mechanisms leading to liver failure and to determine the utility of interleukin-6 (IL-6) administration to improve outcomes. Mice were injected with Chinese hamster ovary cells expressing human IL-6 or no recombinant protein, or were administered recombinant IL-6 or carrier by osmotic mini-pump. Mice were then subjected to 70% or 87% hepatectomy. Light and electron microscopy of liver sections after 87% hepatectomy showed ballooning hepatocytes, vacuolar changes, and mitochondrial abruption, with absence of anoikic nuclei. No significant activation of executor caspases or DNA laddering was observed, although a dramatic decrease in cellular adenosine triphosphate (ATP) stores was measured, suggesting cell death was by a necrotic pathway involving mitochondrial dysfunction. A large increase in protein oxidation was observed, indicative of significant oxidative stress. IL-6 treatment before 87% hepatectomy resulted in less biochemical and histological evidence of liver injury as well as earlier proliferating chain nuclear antigen (PCNA) expression and accelerated recovery of liver mass. IL-6 pretreatment induced the antioxidative injury proteins, ref-1 and GPX1, decreased protein oxidation, vacuolar changes and leakage of mitochondrial products, improved ATP stores, and maintained cellular ultrastructure after 87% hepatectomy. Conclusion: Massive oxidative injury and mitochondrial dysfunction occurs in the liver after extreme hepatectomy. IL-6 improves recovery and survival from extreme liver resection by enhancing pro-growth pathways, reducing oxidative stress, and maintaining mitochondrial function. (HEPATOLOGY 2007;46:802-812.)

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“…Hepatocellular carcinoma (HCC), which is one of the most prevalent life-threatening human cancers, is showing an increased incidence worldwide [Thorgeirsson and Grisham, 2002;Moradpour and Blum, 2005;McKillop et al, 2006]. HCC represents 85% of all liver cancers and is an aggressive disease [McKillop et al, 2006;Hussain et al, 2007].…”

Section: Introductionmentioning

confidence: 99%

“…HCC represents 85% of all liver cancers and is an aggressive disease [McKillop et al, 2006;Hussain et al, 2007]. The most prominent etiological factors associated with HCC are chronic viral hepatitis B and C infections, exposure to environmental chemicals and alcohol, and metabolic liver diseases [Moradpour and Blum, 2005;McKillop et al, 2006]; however, the molecular and cellular mechanisms of HCC pathogenesis are still poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Epigenetic aspects of genotoxic and non‐genotoxic hepatocarcinogenesis: Studies in rodents

Pogribny

Rusyn

Beland

2007

Environ and Mol Mutagen

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Hepatocellular carcinoma, which is one of the most prevalent life-threatening human cancers, is showing an increased incidence worldwide. Recent evidence indicates that the development of hepatocellular carcinoma is associated with not only genetic alterations, but also with profound epigenetic changes. This review summarizes the current knowledge about epigenetic alterations during rodent hepatocarcinogenesis, considers the similarities and differences in epigenetic effects of genotoxic and non-genotoxic rodent liver carcinogens, and discusses the possible role of these effects in the causality of liver tumor development. Environ. Mol. Mutagen. 49:9-15, 2008.

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Molecular Pathogenesis of Hepatocellular Carcinoma

Cited by 95 publications

References 104 publications

The XRCC1 Arg399Gln Genetic Polymorphism Contributes to Hepatocellular Carcinoma Susceptibility: An Updated Meta-analysis

The XRCC1 Arg399Gln Genetic Polymorphism Contributes to Hepatocellular Carcinoma Susceptibility: An Updated Meta-analysis

Interleukin-6 inhibits oxidative injury and necrosis after extreme liver resection

Epigenetic aspects of genotoxic and non‐genotoxic hepatocarcinogenesis: Studies in rodents

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