Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2116658 | Cancer Letters | 2008 | 7 Pages |
Abstract
The risk of hepatocellular carcinoma (HCC) increases with the severity of hepatic inflammation. Interleukin (IL)-1β and tumor necrosis factor (TNF)-α are proinflammatory cytokines with multiple biological effects and may play essential roles in inflammation-linked tumor development. We conducted a case-control study including 209 incident HCC cases and two control groups (275 hospital controls and 381 patients with chronic liver disease [CLD] without HCC) to investigate whether IL-1B and TNF-A gene polymorphisms influence HCC susceptibility with any interaction with alcohol and tobacco. By comparing HCC cases with CLD patients, we found that IL-1B â31T/C polymorphism was associated with HCC risk among never drinkers and current smokers; adjusted odds ratios (and 95% confidence intervals) for C/T and T/T genotypes compared with C/C genotype were 1.70 (0.76-3.77) and 2.46 (1.05-5.76) (P trend = 0.03), respectively, among never drinkers, and 1.53 (0.60-3.99) and 2.54 (0.81-7.95) (P trend = 0.11), respectively, among current smokers. Similarly, HCC risk associated with heavy alcohol intake and current smoking differed by this polymorphism among CLD patients. IL-1B â31T/C polymorphism may modify HCC risk in relation to alcohol intake or smoking.
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Authors
Tatsuhiko Sakamoto, Yasuki Higaki, Megumi Hara, Masayoshi Ichiba, Mikako Horita, Toshihiko Mizuta, Yuichiro Eguchi, Tsutomu Yasutake, Iwata Ozaki, Kyosuke Yamamoto, Shingo Onohara, Seiji Kawazoe, Hirohisa Shigematsu, Shunzo Koizumi, Keitaro Tanaka,