Systematic review: outcome of compensated cirrhosis due to chronic hepatitis C infection

Alazawi, William; Cunningham, Morven; Dearden, Janet; Foster, Graham R.

doi:10.1111/j.1365-2036.2010.04370.x

Cited by 175 publications

(137 citation statements)

References 31 publications

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“…The mean age of the participants included in our study was 60.29 ± 11.19 years, and more than 60% of them had an F4 degree of fibrosis, which may justify the occurrence of HCC in these cases. The risk of HCC development in patients with compensated cirrhosis in our study group is consistent with literature data [3] . However, in spite of the HCC occurrence, SVR was achieved in all the patients that continued antiviral therapy.…”

Section: Discussionsupporting

confidence: 82%

“…It is estimated that, within 20 years of viral infection, about 20%-30% of subjects will develop LC [2] . There is evidence that 2.8%-11.7% of the patients with compensated LC will develop hepatic decompensation sooner or later; as for the incidence of HCC, a percentage of 1.8%-8.3% has been reported [3] . The use of pegylated interferon (IFN) in combination with ribavirin, in treating the HCV infection, leads to a sustained virological response (SVR) in about 50% of patients and it is known to have significant side effects [4] .…”

Section: Introductionmentioning

confidence: 99%

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Hepatocellular carcinoma in the setting of Interferon-free treatment for chronic HCV hepatitis - experience of a single center

Iliescu¹,

Mercan-Stanciu²,

Toma³

et al. 2018

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Aim:This study aims to analyze the particularities of hepatitis C induced hepatocellular carcinoma (HCC), developed during or after treatment with direct-acting antivirals. Methods:We conducted an observational prospective study on 278 patients, who underwent treatment for hepatitis C related liver cirrhosis and respectively for F3 chronic hepatitis C. Liver status was assessed using biological parameters and imagistic evaluation (ultrasonography, computed tomography scan, magnetic resonance imaging). Results:The follow-up time was 14 months. Before therapy, 69.3% of the cirrhotic patients and 26.7% of those with F3 degree of liver fibrosis had high levels of alpha-fetoprotein, with no imagistic evidence of HCC. During treatment, HCC was confirmed in 5 patients, 2 of them presenting portal vein thrombosis (PVT). Antiviral therapy was not interrupted. Two patients developed HCC at the end of treatment, while 4 of them were diagnosed with HCC after three months of ending the treatment. Excepting the ones with PVT, all patients underwent trans-arterial chemoembolization. Conclusion:All patients acquired sustained virological response. The screening for HCC should not be stopped after achievement of sustained virological response. Patients who develop HCC after antiviral treatment often need to be evaluated by magnetic resonance imaging in order to detect the extension of the disease.

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Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Hepatocellular carcinoma in the setting of Interferon-free treatment for chronic HCV hepatitis - experience of a single center

Iliescu¹,

Mercan-Stanciu²,

Toma³

et al. 2018

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“…In recent years, in line with the rising morbidity of hepatitis C virus infection, the incidence of HCC is increasing in many western countries including the United States (4)(5)(6). At present, due to the high recurrence rate and early metastasis, the prognosis of the HCC patients remains very poor (7,8).…”

Section: Introductionmentioning

confidence: 99%

ACK1 promotes hepatocellular carcinoma progression via downregulating WWOX and activating AKT signaling

Xie

Zen

Wang

et al. 2015

International Journal of Oncology

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Abstract. Several studies have revealed that ACK1 is upregulated in various cancers and promotes tumor progression. However, the role and mechanism of ACK1 in hepatocellular carcinoma (HCC) remains unknown. In this study, the expression of ACK1 was assessed in several cell lines and 150 pairs of HCC and adjacent noncancerous liver tissues. The protein expression of p-ACK1 and WWOX were detected by immunohistochemistry to evaluate their correlation with ACK1. Flow cytometry, caspase 3/7 activity assay, BrdU cell proliferation assay, MTT assay and Transwell assay were used to detect apoptosis, proliferation, invasion and migration of HCC cells. The regulatory effect of ACK1 on WWOX, AKT, p-AKT, MMP2 and MMP9 in HCC cells was confirmed by immuno blotting. We found that ACK1 was more highly expressed in HCC tissues than in non-HCC tissues, and over expression of ACK1 was correlated with clinicopathological features of poor prognosis. Clinical analysis demonstrated that ACK1 is an independent prognostic marker for predicting overall survival and disease-free survival of HCC patients. Pearson's correlation coefficient analysis indicated that ACK1 was positively associated with p-ACK1 and was negatively associated with WWOX expression. In vitro studies showed that knockdown of ACK1 promoted HCC cell apoptosis and repressed HCC cells invasion, migration and proliferation. Furthermore, knockdown of ACK1 resulted in upregulation of WWOX and inactivation of AKT signaling. In this study, we also found that knockdown of ACK1 resulted in the downregulation of MMP2 and MMP9 in HCC. Our results indicate that ACK1 is an independent prognostic marker and promotes HCC progression via downregulating WWOX and activating AKT signaling.

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“…The majority of HCC patients have an established background of chronic liver disease (17), and the presence of liver cirrhosis is the main risk factor for the development of HCC (18,19). In addition, HCC is the leading cause of death among patients with cirrhosis (20). Hepatic stellate cells (HSCs), the versatile mesenchymal cells in the liver parenchyma, are vital to the liver's response to inflammation.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of hepatic stellate cells against cisplatin-induced apoptosis in human hepatoma G2 cells

Zhang¹,

Qiao

et al. 2015

International Journal of Oncology

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Abstract. The effects of hepatic stellate cells (HSCs) on tumorigenicity of HCC have been previously reported. However, the detailed mechanisms responsible for these effects remain unclear. In this study, we investigated the effects of HSCs on cisplatin-induced apoptosis in human hepatoma HepG2 cell lines. HepG2 cells were treated with cisplatin alone or co-cultured with LX-2 cells 3 days before incubation with cisplatin. Cisplatin causes apoptosis in HepG2 cells and LX-2 cells protect HepG2 cells from death. The protection of LX-2 cells against cisplatin-induced cytotoxicity in HepG2 cells appeared to be related to the inhibition of apoptosis, as determined by cytotoxicity assay and nuclear staining analysis. p53 and Bax mRNA levels were elevated, and cell cycle arrest was produced after cisplatin treatment. LX-2 cells suppressed this elevation of p53 and Bax as well as the cell cycle arrest induced by cisplatin, when compared with those of the treated cells with cisplatin alone. The LX-2 cells pretreatment inhibited the cisplatin-induced apoptosis, which was related with the incomplete blockage in p53 activation.In summary, the results of our present study demonstrate that HSCs protect HepG2 cells against cisplatin-induced apoptosis and its protective effects occur via inhibiting the activation of p53, which is of critical importance for enhanced understanding of fundamental cancer biology. IntroductionHepatocellular carcinoma (HCC) is the sixth most frequently diagnosed cancer and the third most common leading cause of cancer-related death worldwide, and the burden of this devastating cancer is expected to increase in coming years (1,2). The majority of patients are diagnosed at advanced stage and thus not in a position for curative treatments (3), which have very limited options, and the only systemic therapy currently approved is sorafenib, an oral tyrosine kinase inhibitor drug targeting multiple signalling pathways. The objective response rate (ORR), however, was poor (4). Cisplatin is a widely used anticancer agent and has a broad range of antitumor activity, which is likely a result of inhibition of replication by cisplatin-DNA adducts and induction of apoptosis (5). HCC is considered a poor responder to chemotherapy and a standard systemic treatment does not exist for patients for whom sorafenib is unsuitable or unavailable. The reason could be the frequently observed development of multidrug tumor resistance, which is related to the high expression of the multidrug-resistance gene (6-9). The progression of cancer is no longer recognized as an independent event which only relates to the genetic mutation and uncontrollable growth of cancer cells. New therapeutic strategies are urgently needed, and these will most likely result from a better understanding of the cell biology of HCC.The interaction between tumor cells and their microenvironment has been recognized to fundamentally affect tumor progression (10-12). Physiologically, the surrounding microenvironment constitutes an important barrier to cell t...

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Systematic review: outcome of compensated cirrhosis due to chronic hepatitis C infection

Abstract: SUMMARY BackgroundMost studies evaluating chronic hepatitis C virus (HCV) natural history have taken the development of cirrhosis as an end-point.

Cited by 175 publications

References 31 publications

Hepatocellular carcinoma in the setting of Interferon-free treatment for chronic HCV hepatitis - experience of a single center

Hepatocellular carcinoma in the setting of Interferon-free treatment for chronic HCV hepatitis - experience of a single center

ACK1 promotes hepatocellular carcinoma progression via downregulating WWOX and activating AKT signaling

Protective effects of hepatic stellate cells against cisplatin-induced apoptosis in human hepatoma G2 cells

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