scholarly journals Hepatitis C virus and other risk factors in hepatocellular carcinoma

2012 ◽  
Vol 56 (03) ◽  
pp. 235-240 ◽  
Author(s):  
E. SCHIEFELBEIN ◽  
A.-R. ZEKRI ◽  
D. W. NEWTON ◽  
G. A. SOLIMAN ◽  
M. BANERJEE ◽  
...  
Keyword(s):  
Risk Factors ◽  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C

scholarly journals Epidemiology of Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) Related Hepatocellular Carcinoma

2018 ◽  
Vol 12 (1) ◽  
pp. 26-32 ◽  
Author(s):  
Arnolfo Petruzziello
Keyword(s):  
Risk Factors ◽  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hbv Infection ◽  
Sub Saharan Africa ◽  
Liver Cancers ◽  
B Virus

Introduction:Hepatocellular carcinoma (HCC) is one of the most prevalent primary malignant tumors and accounts for about 90% of all primary liver cancers. Its distribution varies greatly according to geographic location and it is more common in middle and low- income countries than in developed ones especially in Eastern Asia and Sub Saharan Africa (70% of all new HCCs worldwide), with incidence rates of over 20 per 100,000 individuals.Explanation:The most important risk factors for HCC are Hepatitis B Virus (HBV) infection, Hepatitis C Virus (HCV) infection, excessive consumption of alcohol and exposition to aflatoxin B1. Its geographic variability and heterogeneity have been widely associated with the different distribution of HBV and HCV infections worldwide.Chronic HBV infection is one of the leading risk factors for HCC globally accounting for at least 50% cases of primary liver tumors worldwide. Generally, while HBV is the main causative agent in the high incidence HCC areas, HCV is the major etiological factor in low incidence HCC areas, like Western Europe and North America.Conclusion:HBV-induced HCC is a complex, stepwise process that includes integration of HBV DNA into host DNA at multiple or single sites. On the contrary, the cancerogenesis mechanism of HCV is not completely known and it still remains controversial as to whether HCV itself plays a direct role in the development of tumorigenic progression.

Risk Factors for Recurrence after Resection of Hepatitis C Virus-related Hepatocellular Carcinoma

2000 ◽  
Vol 24 (12) ◽  
pp. 1559-1565 ◽  
Author(s):  
Shoji Kubo ◽  
Kazuhiro Hirohashi ◽  
Hiromu Tanaka ◽  
Tadashi Tsukamoto ◽  
Taichi Shuto ◽  
...  
Keyword(s):  
Risk Factors ◽  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Risk Factors For Recurrence

scholarly journals Trends in Incidences and Risk Factors for Hepatocellular Carcinoma and Other Liver Events in HIV and Hepatitis C Virus–coinfected Individuals From 2001 to 2014: A Multicohort Study

2016 ◽  
Vol 63 (6) ◽  
pp. 821-829 ◽  
Author(s):  
Lars I. Gjærde ◽  
Leah Shepherd ◽  
Elzbieta Jablonowska ◽  
Adriano Lazzarin ◽  
Mathieu Rougemont ◽  
...  
Keyword(s):  
Risk Factors ◽  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C

scholarly journals Molecular Pathogenesis of Hepatocellular Carcinoma

2007 ◽  
Vol 10 (2) ◽  
pp. 15-22 ◽  
Author(s):  
S Metodieva
Keyword(s):  
Risk Factors ◽  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Hepatitis B Virus ◽  
Tumor Suppressor ◽  
Hepatitis B ◽  
Aflatoxin B1 ◽  
Molecular Pathogenesis ◽  
B Virus

Molecular Pathogenesis of Hepatocellular CarcinomaThe most important risk factors for the development of human hepatocellular carcinoma (HCC) are chronic infection with hepatitis B virus (HBV) and/or hepatitis C virus (HCV), high dietary exposure to hepatic carcinogen aflatoxin B1 and alcohol abuse. Hepatitis B virus exerts its effects through integration of the viral DNA into the hepatocyte genome, or through acting as transcriptional regulator for several cellular proto-oncogenes and tumor-suppressor genes. Hepatitis C virus may affect hepatocytes via the transcriptional regulation activity of the HCV core protein or via the HCV non structural proteins NS5A, NS5B and NS2, interfering with the regulation of cell cycle and apoptosis. Environmental exposure to aflatoxin B1 can cause a specific missense mutation in codon 249 of the p53 tumor-suppressor gene. Habitual alcohol consumption leads to production of reactive oxygen species and peroxidation damage to DNA. The objective of this review is to make you acquainted with the most common risk factors and the most frequent genetic aberrations associated with the development of HCC.

Response to interferon therapy affects risk factors for postoperative recurrence of hepatitis C virus-related hepatocellular carcinoma

2008 ◽  
Vol 98 (5) ◽  
pp. 358-362 ◽  
Author(s):  
Takahiro Uenishi ◽  
Shuhei Nishiguchi ◽  
Shogo Tanaka ◽  
Takatsugu Yamamoto ◽  
Shigekazu Takemura ◽  
...  
Keyword(s):  
Risk Factors ◽  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Interferon Therapy ◽  
Postoperative Recurrence

scholarly journals Mortality rates and risk factors in 1412 Japanese patients with decompensated hepatitis C virus-related cirrhosis: a retrospective long-term cohort study

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shunichiro Fujiyama ◽  
Norio Akuta ◽  
Hitomi Sezaki ◽  
Mariko Kobayashi ◽  
Yusuke Kawamura ◽  
...  
Keyword(s):  
Risk Factors ◽  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Filtration Rate ◽  
Estimated Glomerular Filtration Rate ◽  
Survival Rates ◽  
Japanese Patients ◽  
Independent Risk Factors

Abstract Background Hepatitis C virus is the leading cause of liver cirrhosis and hepatocellular carcinoma in Japan. We aimed to examine the long-term (> 20 years) mortality and hepatocellular carcinoma rates and associated risk factors in 1412 Japanese patients with decompensated hepatitis C virus-related cirrhosis (Child–Pugh B or C). Methods Cumulative survival and hepatocellular carcinoma rates were determined using Kaplan–Meier analysis. Independent risk factors were identified by multivariate analysis. A two-tailed P-value of < 0.05 was considered significant. Results The patients were followed up for a median of 2 years (range 0.5–24.2 years). In total, 62.3%, 41.7%, 4.7%, and 68.3% of the patients had a history of hepatocellular carcinoma, ascites, hepatic encephalopathy, and esophageal varices, respectively. The 1-, 5-, 10-, and 20-year cumulative overall survival rates in the total cohort was 74.9%, 29.0%, 9.1%, and 1.4%, respectively. The 1-, 3-, 5-, and 10-year cumulative survival rates for patients without hepatocellular carcinoma were 93.1%, 54.4%, 18.2%, and 4.0%, respectively, and the corresponding cumulative post-decompensation hepatocellular carcinoma rates were 14.0%, 31.6%, 46.1%, and 66.2%, respectively. The independent risk factors for mortality were older age, Child–Pugh C cirrhosis, the presence of hepatocellular carcinoma, low estimated glomerular filtration rate, low serum sodium level, low platelet count, and high γ-glutamyl transferase and α-fetoprotein levels for all patients and older age, Child–Pugh C cirrhosis, and low estimated glomerular filtration rate for patients without hepatocellular carcinoma. Overall, 1035 patients (73.3%) died; the causes of death were liver failure with/without hepatocellular carcinoma, pneumonia, sepsis, cardiovascular disease, and non-hepatocellular carcinoma malignancies. The corresponding morality rates per person-year were 133.4, 59.9, 10.9, 10.6, 9.0, and 5.2, respectively. Conclusions Among Japanese patients with decompensated hepatitis C virus-related cirrhosis, hepatocellular carcinoma is associated with poor prognosis. Our results highlight the importance of managing liver-related events, including hepatocellular carcinoma, in these patients.

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