Childhood hepatocellular carcinoma develops exclusively in hepatitis B surface antigen carriers in three decades in Taiwan

Hsu, Hey-Chi; Wu, Mu-Zon; Chang, Mei–Hwei; Su, Ih‐Jen; Chen, Ding‐Shinn

doi:10.1016/s0168-8278(87)80030-2

Cited by 81 publications

(45 citation statements)

References 30 publications

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“…Patients with chronic HBV infection undergo variable clinical courses and have different outcomes. One such outcome is the development of HCC in children after a relatively short period of HBV infection; they are mostly HBV e antigen (HBeAg) negative and anti-HBe positive at the diagnosis of HCC (2). However, the key risk factors responsible for HCC development, particularly the early onset of HCC in children, remain largely unclear.…”

Section: Hronic Hepatitis B Virus (Hbv) Infection Which Poten-mentioning

confidence: 99%

Pre-S2 Deletions of Hepatitis B Virus and Hepatocellular Carcinoma in Children

et al. 2010

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ABSTRACT:The cause of early oncogenesis in hepatitis B virus (HBV)-related childhood hepatocellular carcinoma (HCC) remains unclear. This study investigated whether pre-S deletion of HBV is related to childhood HCC. By using nested polymerase chain reaction, we compared the pre-S sequence of HBV from sera of children with HCC against control children with similar chronic HBV infection. The HBV in sera of children with HCC had a significantly higher rate of pre-S deletion than that of children with chronic HBV infection (p ϭ 0.008). All except one of the pre-S deletions from the HCC group involved the pre-S2 region, whereas no pre-S2 deletion was found in the chronic HBV group (p ϭ 0.003). There was a trend whereby genotype-C sera had a higher rate of pre-S2 deletion than genotype-B sera (p ϭ 0.11). A multivariate logistic regression model revealed that pre-S deletion was an independent risk factor for HCC in children (odds ratio: 36.69, p ϭ 0.015). In conclusion, pre-S2 deletion does not need to take decades to occur; its presence in nearly half of children with HCC, in contrast to its absence in children with chronic HBV infection, suggests a link between pre-S2 deletion and HCC development in children. (Pediatr Res 67: 90-94, 2010)

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Section: Hronic Hepatitis B Virus (Hbv) Infection Which Poten-mentioning

confidence: 99%

Pre-S2 Deletions of Hepatitis B Virus and Hepatocellular Carcinoma in Children

et al. 2010

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“…This multistep nature of carcinogenesis has been described in well-developed models of chemical hepatocarcinogenesis (84,85,310), as well as in sporadic carcinogenesis of other solid tumors (217). In this regard, there have been several reports in the literature documenting the presence of PHC in HBV-infected children (46,153,172,260,355,404,405). The relatively short incubation time for PHC in children is consistent with the hypothesis that these children have a genetic predisposition for the development of such tumors.…”

Section: Putative Cellular and Molecular Modelsmentioning

confidence: 93%

“…Integration of hepadnavirus DNA in PHC cells from chronically infected woodchucks (329,330,338), ground squirrels (212,215), and ducks (159,413) has also been documented, demonstrating the generality of this property among these viruses. Integration of HBV at multiple sites within the host genome occurs early after infection (19,29,47,153,172,355,404). These observations imply that one or more integrated species may carry out functions important to the initiation and/or maintenance of PHC.…”

Section: Putative Cellular and Molecular Modelsmentioning

confidence: 99%

Hepatitis B virus infection and primary hepatocellular carcinoma

Feitelson

1992

Clin Microbiol Rev

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For many years, epidemiological studies have demonstrated a strong link between chronic hepatitis B virus (HBV) infection and the development of primary hepatocellular carcinoma (PHC). Other hepatocarcinogens such as hepatitis C virus and aflatoxin also contribute to hepatocarcinogenesis either in conjunction with HBV infection or alone. Cellular and molecular biological studies are providing explanations for the HBV-PHC relationship, and models are now being formulated to further test the relative importance of various factors such as viral DNA integration, activation of oncogenes, genetic instability, loss of tumor suppressor genes, and trans-activating properties of HBV to the pathogenesis of PHC. Further research will probably define more than a single mechanism whereby chronic HBV infection results in PHC.

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“…In 1987, two studies showed that HBsAg was positive in 100% of childhood HCC in Taiwan. 56,57 Therefore, there is a chance that the effects of hepatitis B vaccination might be disclosed earlier by studying HCC in children. Dr. Mei-Hwei Chang, my pediatric team member, took this opportunity and made seminal discoveries.…”

Section: Effectiveness Of Mass Hepatitis B Vaccination In the Decreasmentioning

confidence: 99%

Fighting against viral hepatitis: Lessons from Taiwan

Chen

2011

Hepatology

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Viral hepatitis and its sequelae are important health problems worldwide, including Taiwan. For the last 40 years, Taiwan's scientists and health care providers have worked hard to control these sequelae, and the results have been excellent. The author, Ding-Shinn Chen, had a key role in planning and establishing the control program in Taiwan, and participated in the endeavors from the very beginning. In this perspective, he describes how he became interested in research as a medical student, his encounters with hepatitis B and C, how he and his colleagues started early detection of hepatocellular carcinoma (HCC), how he helped Taiwan's government create and implement the Viral Hepatitis Control Program, and how the effectiveness of the program in the decrease of hepatitis B carriage and HCC was monitored. He also discusses how he pioneered the use of interferon-α plus ribavirin to treat chronic hepatitis C. Hepatitis B viral load as a risk factor for HCC and cirrhosis in hepatitis B surface antigen carriers is reviewed briefly, as is the prevention of sequelae by antiviral therapies. Finally, Dr. Chen discusses unresolved issues that must be addressed and predicts the changes of the patterns of liver disease in Taiwan beyond the mid-21st century, which is in part affected by the fight against viral hepatitis that was initiated in the early 1980s. Conclusion : Dr. Chen's perspective illustrates Taiwan's fight against viral hepatitis over the last 40 years. This experience can be shared by other countries in which the disease is equally prevalent. (Hepatology 2011;)

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Childhood hepatocellular carcinoma develops exclusively in hepatitis B surface antigen carriers in three decades in Taiwan

Cited by 81 publications

References 30 publications

Pre-S2 Deletions of Hepatitis B Virus and Hepatocellular Carcinoma in Children

Pre-S2 Deletions of Hepatitis B Virus and Hepatocellular Carcinoma in Children

Hepatitis B virus infection and primary hepatocellular carcinoma

Fighting against viral hepatitis: Lessons from Taiwan

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