Hepatitis B Vaccination and Hepatocellular Carcinoma Rates in Boys and Girls

Chang, Mei–Hwei; Shau, Wen–Yi; Chen, Chien-Jen; Wu, Tzee–Chung; Kong, Man‐Shan; Liang, Der‐Cherng; Hsu, Hsu‐Mei; Chen, Huey‐Ling; Hsu, Hong–Yuan; Chen, Ding‐Shinn

doi:10.1001/jama.284.23.3040

Cited by 179 publications

(95 citation statements)

References 12 publications

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“…This supports the role of HBV vaccination in preventing HCC in HBV endemic areas [32]. Strikingly, if AFB1 exposure was balanced, the order (from high to low) in the increment of PCC per fmol of AAA in age and gender matched groups was HCC > cAb/sAg > null > sAb (Figure 3), suggesting that HBV infection alone significantly increased oxidative stress.…”

Section: Discussionsupporting

confidence: 60%

Hepatitis B virus infection contributes to oxidative stress in a population exposed to aflatoxin B1 and high-risk for hepatocellular carcinoma

Liu

Peng

et al. 2008

Cancer Letters

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Biomarkers of Hepatitis B Virus (HBV) infection, aflatoxin B1 (AFB1) exposure and oxidative stress were detected in 71 hepatocellular carcinoma (HCC) patients and 694 controls from southern China. Plasma level of AFB1-Albumin-Adducts (AAA) and protein carbonyl content (PCC) were significantly higher in the 71 HCC cases than in any age/gender matched HBV sero-status groups (P<0.001). HCC patients positive for the p53-249 G-T mutation had a marginally higher level of PCC than those negative for the mutation (p=0.077). HBV infection had a prominent influence on the association between AFB1 exposure and oxidative stress biomarkers in the controls. Our study indicates a significant contribution from HBV infection to oxidative stress in a population with AFB1 exposure which might substantially increase risk for HCC in this region.

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Section: Discussionsupporting

confidence: 60%

Hepatitis B virus infection contributes to oxidative stress in a population exposed to aflatoxin B1 and high-risk for hepatocellular carcinoma

Liu

Peng

et al. 2008

Cancer Letters

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“…seroconversion at [16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][30][31][32][33][34][35][36][37][38][39][40], and >40 years of age, respectively. 5,6 These differences may be attributable to differences in the studied cohorts.…”

Section: Discussionmentioning

confidence: 99%

“…13,14 The relative risks of HBV-related hepatocellular carcinoma and liver disease-related death were consistently severalfold higher in males than in females. [15][16][17][18] However, the relationship between HBV genotype, gender, and HBeAg-negative hepatitis remains controversial. 5,6,19 Prior nucleos(t)ide analogue treatment was also reported as a risk factor for hepatitis reactivation after HBeAg seroconversion, but the differences among various antiviral agents are unclear.…”

mentioning

confidence: 99%

Predictors of hepatitis B e antigen‐negative hepatitis in chronic hepatitis B virus‐infected patients from childhood to adulthood

Chiu

Chang

et al. 2015

Hepatology

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Hepatitis B e antigen (HBeAg)-negative hepatitis is a clinical indicator of poor outcome for chronic hepatitis B viral (HBV) infection. This long-term prospective cohort study aimed to elucidate the predictors of developing HBeAg-negative hepatitis in chronic HBV-infected subjects followed from childhood to adulthood. We followed 434 HBeAgpositive chronic HBV-infected patients from a median age of 7.22 years (interquartile range 4.31-10.21 years). Spontaneous HBeAg seroconversion occurred in 359 subjects at a median age of 13.93 years (interquartile range 8.76-20.59 years), and 75 subjects developed HBeAg seroconversion after antiviral therapy. These patients were followed for a median of 14.40 years (interquartile range 6.14-22.02 years) after HBeAg seroconversion. Clinical data were analyzed to delineate the predictors of developing HBeAgnegative hepatitis. The HBV basal core promoter and precore/core gene sequences were also evaluated in subjects with and without HBeAg-negative hepatitis. The overall annual incidence of HBeAg-negative hepatitis was 0.37% (95% confidence internal 0.35-0.39) in spontaneous HBeAg seroconverters. The overall annual incidence of HBeAg-negative hepatitis increased to 2.64% in lamivudine-treated subjects but did not increase in those treated with interferon-alpha (0.58%). Male gender (hazard ratio 5 3.15), HBV genotype C (hazard ratio 5 4.40), HBeAg seroconversion after 18 years of age (hazard ratio 5 2.46), and lamivudine therapy prior to HBeAg seroconversion (hazard ratio 5 1.42) were predictors of HBeAg-negative hepatitis in HBeAg seroconverters (P < 0.05). HBeAg-negative hepatitis subjects carried more A1762T/G1764A, C2063A, and A2131C HBV gene mutations than those without HBeAg-negative hepatitis. Conclusions: HBeAg seroconversion during childhood predicts a lower risk of HBeAgnegative hepatitis in later life. Interferon-alpha therapy may be an effective antiviral therapy beneficial in chronic HBV-infected children with severe inflammation that facilitates HBeAg seroconversion in earlier life. (HEPATOLOGY 2016;63:74-82)

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“…Immunoprevention of tumors associated with microbial infections is expected to decrease the human tumor burden in the near future (1,2). Vaccines against tumor antigens with a causal role in the promotion of carcinogenesis unrelated to infections (oncoantigens; ref.…”

Section: Introductionmentioning

confidence: 99%

A DNA Vaccine against ERBB2 Impairs Chemical Carcinogenesis in Random-Bred Hamsters

Berta

Sprio

Iezzi

et al. 2011

Cancer Prevention Research

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Vaccines against oncoantigens halt early neoplastic lesions in several cancer-prone, genetically engineered mouse models, whereas their ability to prevent chemical carcinogenesis has not been explored. This is a significant issue, as exposure to chemical mutagens is responsible for a substantial percentage of cancers worldwide. Here, we show that the archetypal oncoantigen ERBB2 is transiently overexpressed in Syrian hamsters during the early stages of 7,12-dimethylbenz[a]anthracene (DMBA)-induced oral carcinogenesis. Repeated DNA vaccinations against ERBB2 significantly reduce the number, size, and severity of oral lesions in a manner directly proportional to the anti-ERBB2 antibody response. These results support the prospects of vaccines as a fresh strategy in the management of individuals at risk for exposure to defined carcinogenic agents. Cancer Prev Res; 4(7); 994-1001. Ó2011 AACR.

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Hepatitis B Vaccination and Hepatocellular Carcinoma Rates in Boys and Girls

Abstract: Our results suggest that boys may benefit more from HBV vaccination than girls in the prevention of HCC.

Cited by 179 publications

References 12 publications

Hepatitis B virus infection contributes to oxidative stress in a population exposed to aflatoxin B1 and high-risk for hepatocellular carcinoma

Hepatitis B virus infection contributes to oxidative stress in a population exposed to aflatoxin B1 and high-risk for hepatocellular carcinoma

Predictors of hepatitis B e antigen‐negative hepatitis in chronic hepatitis B virus‐infected patients from childhood to adulthood

A DNA Vaccine against ERBB2 Impairs Chemical Carcinogenesis in Random-Bred Hamsters

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