title: Green tea consumption, inflammation and the risk of primary hepatocellular carcinoma in a Chinese population.
abstract: OBJECTIVE
  Green tea has been found to possess anti-inflammatory, anti-oxidative and anti-carcinogenic properties. The present study examines the association between green tea drinking and hepatocellular carcinoma (HCC) and its interactions with other risk or protective factors and single nucleotide polymorphisms (SNP) of inflammation and oxidative stress related genes.
  
  
  METHODS
  A population-based case-control study with 204 primary HCC cases and 415 healthy controls was conducted in Taixing, China. Epidemiological data were collected using a standard questionnaire. SNPs of genes of the inflammation and metabolic pathways were genotyped at the UCLA Molecular Epidemiology Laboratory. Logistic regression was performed to estimate adjusted odds ratios and 95% confidence intervals.
  
  
  RESULTS
  Longer duration and larger quantities of green tea consumption were inversely associated with primary HCC. Individuals who drank green tea longer than 30 years were at lowest risk (adjusted OR=0.44, 95% CI: 0.19-0.96) compared with non-drinkers. A strong interaction was observed between green tea drinking and alcohol consumption (adjusted OR for interaction=3.40, 95% CI: 1.26-9.16). Green tea drinking was also observed to have a potential effect modification on HBV/HCV infection, smoking and polymorphisms of inflammation related cytokines, especially for IL-10.
  
  
  CONCLUSIONS
  Green tea consumption may protect against development of primary HCC. Potential effect modifications of green tea on associations between primary HCC and alcohol drinking, HBV/HCV infection, and inflammation-related SNPs were suggested.
authors.affiliation: Department of Social and Preventive Medicine, The State University of New York at Buffalo, NY 14214-8001, USA.
authors.forename: Yanli
authors.initials: Y
authors.lastname: Li
authors.forename: Shen-Chih
authors.initials: SC
authors.lastname: Chang
authors.forename: Binh Y
authors.initials: BY
authors.lastname: Goldstein
authors.forename: William L
authors.initials: WL
authors.lastname: Scheider
authors.forename: Lin
authors.initials: L
authors.lastname: Cai
authors.forename: Nai-Chieh Y
authors.initials: NC
authors.lastname: You
authors.forename: Heather P
authors.initials: HP
authors.lastname: Tarleton
authors.forename: Baoguo
authors.initials: B
authors.lastname: Ding
authors.forename: Jinkou
authors.initials: J
authors.lastname: Zhao
authors.forename: Ming
authors.initials: M
authors.lastname: Wu
authors.forename: Qingwu
authors.initials: Q
authors.lastname: Jiang
authors.forename: Shunzhang
authors.initials: S
authors.lastname: Yu
authors.forename: Jianyu
authors.initials: J
authors.lastname: Rao
authors.forename: Qing-Yi
authors.initials: QY
authors.lastname: Lu
authors.forename: Zuo-Feng
authors.initials: ZF
authors.lastname: Zhang
authors.forename: Lina
authors.initials: L
authors.lastname: Mu
mesh_terms: D000328:Adult; D000368:Aged; D006528:Carcinoma, Hepatocellular / Q000453:epidemiology* / Q000235:genetics; D016022:Case-Control Studies; D002681:China / Q000453:epidemiology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000453:epidemiology / Q000235:genetics; D008113:Liver Neoplasms / Q000453:epidemiology* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D012307:Risk Factors; D013662:Tea; D055815:Young Adult
chemical_list: D013662:Tea