Prevention of Hepatocellular Carcinoma in Patients with Chronic Hepatitis B Virus Infection

Kim, Beom Kyung; Han, Kwang Hyub; Ahn, Sang Hoon

doi:10.1159/000333258

Cited by 50 publications

(46 citation statements)

References 129 publications

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“…(3,4) Hepatitis B virus (HBV) infection, hepatitis C virus (HCV) infection, and chronic exposure to aflatoxin play crucial roles in hepatocarcinogenesis among Asian people, while fatty liver disease and high consumption of alcohol are the dominant causes among low incidence regions. (5,6) The HCC incidence rate is remarkably high in China, accounting for approximately 55% of annual new cases in the world. (7) Particularly in Guangxi province of China, an endemic area of HBV infection, the HCC mortality has risen as the first cause of malignant cancer-relative death.…”

mentioning

confidence: 99%

Comparative proteomic profiles indicating genetic factors may involve in hepatocellular carcinoma familial aggregation

Zhong

Ning

et al. 2012

Cancer Science

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Familial aggregation of hepatocellular carcinoma (HCC), the third leading cause of cancer death worldwide, has shown to be a common phenomenon. We investigated the association between the genetic background and HCC familial aggregation. Serum samples were collected from HCC family members and normal control family members for screening the differentially expressed protein peaks with the approach of surface-enhanced laser desorption ionization time-of-flight mass spectrometry. Potential genetically associated protein peaks were selected and further identified by matrix assisted laser desorption ionization-time of flight mass spectrometry. A panel of six protein peaks (m/z 6432. 94, 8478.35, 9381.91, 17284.67, 17418.34, and 18111.04) were speculated to reflect the genetic susceptibility of HCC familial aggregation. Three of them (m/z 6432.94, 8478.35, and 9381.91) were selected to identify as the candidate proteins. Nine identified proteins, including mostly apolipoprotein family (ApoA1, ApoA2, ApoC3, ApoE) and serum amyloid A protein (SAA), were found overexpressed in the multiple HCC cases family members. The comparative proteomic profiles have suggested that genetic factors ought to be taken into account for familial aggregation of HCC. (Cancer Sci 2012; 103: 1833-1838 H epatocellular carcinoma (HCC) is one of the most commonly diagnosed cancers, and ranks the third cause of cancer related death in the world (9.2% of the total).(1,2) Among different geographical regions, large variation of morbidity and risk factors were observed, with the highest rate in Asian, and lowest rate in the US as well as Europe countries.(3,4) Hepatitis B virus (HBV) infection, hepatitis C virus (HCV) infection, and chronic exposure to aflatoxin play crucial roles in hepatocarcinogenesis among Asian people, while fatty liver disease and high consumption of alcohol are the dominant causes among low incidence regions.(5,6) The HCC incidence rate is remarkably high in China, accounting for approximately 55% of annual new cases in the world.(7) Particularly in Guangxi province of China, an endemic area of HBV infection, the HCC mortality has risen as the first cause of malignant cancer-relative death. (8) It is well-accepted that HBV infection constitutes the main etiological factor of HCC, while the process of hepatocarcinogenesis integrates multi-stages and multi-factors, including interactions of HBV, chemical carcinogen, and genetic susceptibility.(9) In addiction, the literature conveys that the lifetime risk of developing HCC for HBV infected individuals has been estimated to be 40%, (10) implying that a wide individual discrepancy exists in the HCC susceptibility, and that environmental factors alone are insufficient to fully address the familial aggregation of HCC. (11,12) We have observed that most HCC occurs obviously in clusters by geographical distribution or by family aggregation in Guangxi, China. Family aggregation of HCC has received researchers' attention for decades. Pedigree studies are frequently carried out to val...

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confidence: 99%

Comparative proteomic profiles indicating genetic factors may involve in hepatocellular carcinoma familial aggregation

Zhong

Ning

et al. 2012

Cancer Science

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“…Viral factors associated with a greater risk of HCC include HBeAg positivity, serum HBV DNA levels, and HBV genotypes. Increasing evidence suggests that persistent HBV replication is a predictor of HCC [3]. Thus, efforts to prevent HCC in chronic hepatitis B (CHB) patients should begin by controlling HBV infection and resistance to HBV replication maybe more effective.…”

Section: Hcc Is a Potentially Fatal Consequence Of Hbv Infectionmentioning

confidence: 99%

“…When intermediate-to-advanced cancer is found at diagnosis, the majority of HCC patients are eligible only for nonsurgical treatment which is less efficacious. Thus detecting HCC at an earlier stage is important so that the use of curative treatments is possible [3].…”

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confidence: 99%

Decreased expression of Small glutamine-rich tetratricopeptide repeat-containing protein (SGT) correlated with prognosis of Hepatocellular carcinoma

Zhang¹,

Chen²,

He³

et al. 2014

neo

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Small glutamine-rich tetratricopeptide repeat-containing protein (SGT) is an ubiquitously expressed cochaperone of heat shock cognate protein of 70 kDa (Hsc70). SGT binds to the C terminus of Hsc70 to recruit Hsc70 into complexes of diverse function. SGTB was identified as an isoform of SGT with 60% amino acid sequence homology. To investigate the expression of SGTB in hepatocellular carcinoma (HCC) and determine its correlation with tumor progression and prognosis, we evaluated the expression levels of SGTB in HCCs and corresponding adjacent non-tumor liver tissues. We also assessed the association between their expression and clinicopathologic parameters. The expression of SGTB was absent or low in HCCs while it was notable in paracancerous tissues from 108 patients by western blotting and immunochemistry (P < 0.05). Among the 108 HCCs, low expression of SGTB was associated with gender, histological grade (P<0.001) and HBsAg expression (P=0.002). Univariate analysis showed that the low SGTB expression was associated with poor prognosis (P<0.001). Thus, decreased expression of SGTB may be a favorable independent poor prognostic parameter for hepatocellular carcinoma.

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“…The lifetime risk of HBV carriers to develop cirrhosis, liver failure or HCC is estimated to be as high as 15-40% [6,7,8,9]. The prevalence of HBV infection and the age of individuals infected vary largely in different geographic regions, which at least partially accounts for the different prevalence of HCC (fig.…”

Section: Epidemiology Of Hbv Infectionmentioning

confidence: 99%

Direct Effects of Hepatitis B Virus-Encoded Proteins and Chronic Infection in Liver Cancer Development

Ringelhan

Heikenwälder²,

Protzer³

2013

Dig Dis

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Hepatocellular carcinoma (HCC) ranks as the third leading cause of cancer-related death worldwide with currently limited treatment options. Chronic hepatitis B virus (HBV) infection accounts for HCC development in more than 50% of cases. The lifetime risk of HBV carriers to develop cirrhosis, liver failure or HCC is estimated to be as high as 15-40%. Although several pathways and triggers contributing to HCC development have been described, many features of hepatocellular carcinogenesis and the attributed direct role of viral factors remain elusive. Host genetic factors, the geographic area and epidemiologic factors, as well as the direct risk related to chronic HBV and hepatitis C virus (HCV) infections, account for geographical and gender differences of HCC prevalence. There is growing evidence that hepatocarcinogenesis is a multistep process. Human HCC is typically preceded by chronic inflammation and apoptotic and nonapoptotic cell death with compensatory liver proliferation. However, we still lack a thorough understanding of the common underlying molecular mechanisms. High levels of HBV replication and chronicity of inflammation are known to independently increase the risk for HCC. A direct carcinogenic role of viral factors is very likely to contribute to liver cancer since HCC is known to also occur in noncirrhotic livers of individuals with an inactive chronic or even with occult HBV infection with no significant histological signs of inflammation or cytopathic effects. Furthermore, synergistic or independent viral risk factors for primary liver cancer development have been described, such as HBV genotype, integration of viral DNA into the host genome and direct effects of viral proteins. A broader understanding of these viral factors in hepatocarcinogenesis might give rise to new diagnostic and therapeutic means in the future. We review the current state of research in liver cancer development and focus on the role of direct viral factors in HBV infection.

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Prevention of Hepatocellular Carcinoma in Patients with Chronic Hepatitis B Virus Infection

Cited by 50 publications

References 129 publications

Comparative proteomic profiles indicating genetic factors may involve in hepatocellular carcinoma familial aggregation

Comparative proteomic profiles indicating genetic factors may involve in hepatocellular carcinoma familial aggregation

Decreased expression of Small glutamine-rich tetratricopeptide repeat-containing protein (SGT) correlated with prognosis of Hepatocellular carcinoma

Direct Effects of Hepatitis B Virus-Encoded Proteins and Chronic Infection in Liver Cancer Development

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