Plasma Carotenoids, Glutathione S-Transferase M1 andT1 Genetic Polymorphisms, and Risk of Hepatocellular Carcinoma: Independent and Interactive Effects

Yu, Ming‐Whei; Chiu, Yueh‐Hsia; Chiang, Yi-Ching; Chen, Chien‐Hung; Lee, Tzong‐Hsi; Santella, Regina M.; Chern, Herng-Der; Liaw, Yun–Fan; Chen, Chien-Jen

doi:10.1093/oxfordjournals.aje.a009862

Cited by 73 publications

(45 citation statements)

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“…CYP1A1 is involved in the metabolic activation of PAHs, and low plasma carotenoid level has been shown to modify the smoking-related risk of HCC. 10,35 *In analysis of the joint effect of chronic liver disease and the p53 polymorphism on HCC, age, cigarette smoking, alcohol drinking, GSTM1, and CYP1A1 MspI genotypes, as well as family history of HCC were also included in the logistic regression model. In analysis of the joint effect of family history of HCC and the p53 polymorphism, age, cigarette smoking, alcohol drinking, GSTM1, and CYP1A1 MspI genotypes, as well as chronic liver disease were also included in the regression model for adjusting their effects.…”

Section: Resultsmentioning

confidence: 99%

“…Genotyping of GSTM1 and CYP1A1 MspI polymorphisms was performed by polymerase chain reaction-based methods, and prediagnostic plasma levels of ␣-carotene, ␤-carotene, and lycopene were measured by high-performance liquid chromatography as described previously. 4,10,33 Among the 80 HCC cases included in the analyses of the polymorphisms in p53, GSTM1, and CYP1A1, 1 had no available plasma sample. Approximately one half of the 328 control subjects in this study were randomly selected for assay of plasma carotenoids.…”

Section: Subjectsmentioning

confidence: 99%

“…[1][2][3][4][5][6][7][8][9][10] Most genotoxic chemical carcinogens are not intrinsically reactive but require metabolic conversion to DNA-binding intermediates by Phase I enzymes. 11 Activated metabolites of carcinogens formed in Phase I are subjected to metabolic conjugation and other kinds of detoxification by Phase II enzymes.…”

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confidence: 99%

“…12 We previously reported that several polymorphic genes encoding for Phase I (cytochrome P4502E1, CYP2E1) and Phase II enzymes (glutathione S-transferase classes µ and , GST M1, and T1) might be involved in modulating HCC risk in relation to exposure to environmental carcinogens such as aflatoxin B 1 and tobacco smoke. 4,5,9,10 These genes determine the early steps of hepatocarcinogenesis.…”

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Ap53genetic polymorphism as a modulator of hepatocellular carcinoma risk in relation to chronic liver disease, familial tendency, and cigarette smoking in hepatitis B carriers

et al. 1999

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This study evaluated whether the codon 72 p53 polymorphism was related to hepatocellular carcinoma (HCC). Genotypes of p53 were determined in 80 incident cases of HCC and 328 controls nested in a cohort study of 4,841 male chronic hepatitis B carriers. No overall increase in HCC risk with the Pro variant allele of the p53 polymorphism was apparent. However, there were synergistic effects on HCC development for the Pro allele with chronic liver disease and family history of HCC in first-degree relatives. Compared with subjects without the Pro allele and chronic liver disease, the increase in HCC risk associated with chronic liver disease among those without the Pro allele was only threefold. Subjects with both chronic liver disease and the Pro allele were at an increased risk of 7.60 (95% CI ‫؍‬ 2.28-25.31). When subjects without family history of HCC and the Pro allele were considered as the reference group, there was no apparent increased risk of HCC for those without the Pro allele who had family history of HCC. Among those with both factors, there was a significantly increased risk of 3.29 (95% CI ‫؍‬ 1.10-9.85). Both cigarette smoking and glutathione S-transferase M1 genotype modified the risk of HCC associated with the p53 polymorphism. Significantly increased risk associated with the p53 genotype was observed only among smokers who were glutathione S-transferase-null (Pro/Pro vs. Arg/Arg: odds ratio ‫؍‬ 6.46; 95% CI ‫؍‬ 1.55-26.94). The p53 polymorphism also interacted with the cytochrome P450 1A1 and carotenoid levels in smoking-related hepatocarcinogenesis. (HEPATOLOGY 1999;29:697-702.) Chronic infection with hepatitis B virus (HBV) is the major cause of at least 80% of hepatocellular carcinoma (HCC) throughout the world. 1 However, only about one fifth of chronic HBV carriers develop HCC in their lifetime, 2 suggesting that there is interindividual variation in susceptibility to hepatocarcinogenesis.Both viral and chemical carcinogens are involved in the multistage process of human hepatocarcinogenesis.

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Section: Resultsmentioning

confidence: 99%

Section: Subjectsmentioning

confidence: 99%

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Ap53genetic polymorphism as a modulator of hepatocellular carcinoma risk in relation to chronic liver disease, familial tendency, and cigarette smoking in hepatitis B carriers

et al. 1999

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“…Accordingly, retinoids inhibit chemically induced liver cancer in animals (Moreno et al, 2002). In addition, an inverse relationship between the risk of HHC and RA levels has been observed (Yu et al, 1995(Yu et al, , 1999 and the administration of a synthetic retinoid prevented the occurrence of a secondary cancer in patients with HCC (Muto et al, 1999). …”

Section: Interaction With Retinoidsmentioning

confidence: 99%

Risk factors and mechanisms of hepatocarcinogenesis with special emphasis on alcohol and oxidative stress

Seitz

Stickel

2006

Biological Chemistry

276

178

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Hepatocellular cancer is the fifth most frequent cancer in men and the eighth in women worldwide. Established risk factors are chronic hepatitis B and C infection, chronic heavy alcohol consumption, obesity and type 2 diabetes, tobacco use, use of oral contraceptives, and aflatoxin-contaminated food. Almost 90% of all hepatocellular carcinomas develop in cirrhotic livers. In Western countries, attributable risks are highest for cirrhosis due to chronic alcohol abuse and viral hepatitis B and C infection. Among those with alcoholic cirrhosis, the annual incidence of hepatocellular cancer is 1-2%. An important mechanism implicated in alcohol-related hepatocarcinogenesis is oxidative stress from alcohol metabolism, inflammation, and increased iron storage. Ethanolinduced cytochrome P-450 2E1 produces various reactive oxygen species, leading to the formation of lipid peroxides such as 4-hydroxy-nonenal. Furthermore, alcohol impairs the antioxidant defense system, resulting in mitochondrial damage and apoptosis. Chronic alcohol exposure elicits hepatocyte hyperregeneration due to the activation of survival factors and interference with retinoid metabolism. Direct DNA damage results from acetaldehyde, which can bind to DNA, inhibit DNA repair systems, and lead to the formation of carcinogenic exocyclic DNA etheno adducts. Finally, chronic alcohol abuse interferes with methyl group transfer and may thereby alter gene expression.

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N‐Acetyltransferase‐2, glutathione S‐transferase M1 and T1 genetic polymorphisms, cigarette smoking and hepatocellular carcinoma: A case‐control study

Gelatti

Covolo

Talamini

et al. 2005

Intl Journal of Cancer

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Our aim was to evaluate the role of N-acetyltransferase (NAT2) and glutathione S-transferase M1 and T1 (GSTM1 and GSTT1) polymorphisms in hepatocellular carcinoma (HCC) according to cigarette smoking, taking into account hepatitis B (HBV) and C (HCV) viral infection as well as alcohol consumption. A hospitalbased case-control study was conducted in 2 areas of north Italy. Cases (n = 200) were patients hospitalized for HCC, and controls (n = 400) were patients admitted for reasons other than liver disease, neoplasms and tobacco-and alcohol-related diseases. Genotypes were determined using PCR and the PCR/restriction fragment length polymorphism-based method. The putative risk genotypes NAT2 slow acetylator, GSTM1 null and GSTT1 null were not associated with HCC (OR = 1.3, 95% CI 0.8-2.0; OR = 1.0, 95% CI 0.6-1.5; OR = 0.8, 95% CI 0.4-1.4, respectively). Although not statistically significant, an increase in HCC risk was observed among light smokers (1-20 pack-years) carrying GSTT1 null (OR = 1.7, 95% CI 0.6-4.7) and NAT2 slow acetylator (OR = 1.3, 95% CI 0.6-3.0) genotypes. In conclusion, there was no evidence for a gene-environment interaction in HCC risk for GSTM1, GSTT1 and NAT2 genotypes. ' 2005 Wiley-Liss, Inc.

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Plasma Carotenoids, Glutathione S-Transferase M1 andT1 Genetic Polymorphisms, and Risk of Hepatocellular Carcinoma: Independent and Interactive Effects

Cited by 73 publications

References 29 publications

Ap53genetic polymorphism as a modulator of hepatocellular carcinoma risk in relation to chronic liver disease, familial tendency, and cigarette smoking in hepatitis B carriers

Ap53genetic polymorphism as a modulator of hepatocellular carcinoma risk in relation to chronic liver disease, familial tendency, and cigarette smoking in hepatitis B carriers

Risk factors and mechanisms of hepatocarcinogenesis with special emphasis on alcohol and oxidative stress

N‐Acetyltransferase‐2, glutathione S‐transferase M1 and T1 genetic polymorphisms, cigarette smoking and hepatocellular carcinoma: A case‐control study

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