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Single nucleotide polymorphisms of 8 inflammation‐related genes and their associations with smoking‐related cancers
Author(s) -
Oh Sam S.,
Chang ShenChih,
Cai Lin,
CordonCardo Carlos,
Ding BaoGuo,
Greenland Sander,
He Na,
Jiang Qingwu,
Kheifets Leeka,
Le Anh,
Lee YuanChin Amy,
Liu Simin,
Lu MingLan,
Mao Jenny T.,
Morgenstern Hal,
Mu LiNa,
Pantuck Allan,
Papp Jeanette C.,
Park Sungshim Lani,
Rao Jian Yu,
Reuter Victor E.,
Tashkin Donald P.,
Wang Hua,
You NaiChieh Y.,
Yu ShunZhang,
Zhao JinKou,
Belldegrun Arie,
Zhang ZuoFeng
Publication year - 2010
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.25214
Subject(s) - medicine , odds ratio , lung cancer , cancer , tobacco smoke , population , gastroenterology , esophagus , case control study , single nucleotide polymorphism , oncology , confidence interval , bladder cancer , pathology , genotype , biology , genetics , gene , environmental health
Tobacco smoke and its metabolites are carcinogens that increase tissue oxidative stress and induce target tissue inflammation. We hypothesized that genetic variation of inflammatory pathway genes plays a role in tobacco‐related carcinogenesis and is modified by tobacco smoking. We evaluated the association of 12 single nucleotide polymorphisms of 8 inflammation‐related genes with tobacco‐related cancers (lung, oropharynx, larynx, esophagus, stomach, liver, bladder, and kidney) using 3 case‐control studies from: Los Angeles (population‐based; 611 lung and 553 upper aero‐digestive tract cancer cases and 1,040 controls), Taixing, China (population‐based; 218 esophagus, 206 stomach, 204 liver cancer cases, and 415 controls), and Memorial Sloan‐Kettering Cancer Center (hospital‐based; 227 bladder cancer cases and 211 controls). After adjusting for age, education, ethnicity, gender, and tobacco smoking, IL10 rs1800871 was inversely associated with oropharyngeal cancer (CT+TT vs . CC adjusted odds ratio [aOR]: 0.69, 95% confidence interval [CI]: 0.50–0.95), and was positively associated with lung cancer among never smokers (TT vs . CT+CC aOR: 2.5, 95% CI: 1.3–5.1) and inversely with oropharyngeal cancer among ever smokers (CT+TT vs . CC aOR: 0.63, 95% CI: 0.41–0.95). Among all pooled never smokers (588 cases and 816 controls), TNF rs1799964 was inversely associated with smoking‐related cancer (CC vs . CT+TT aOR: 0.36, 95% CI: 0.17–0.77). Bayesian correction for multiple comparisons suggests that chance is unlikely to explain our findings (although epigenetic mechanisms may be in effect), which support our hypotheses, suggesting that IL10 rs1800871 is a susceptibility marker for oropharyngeal and lung cancers, and that TNF rs1799964 is associated with smoking‐related cancers among never smokers.