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In vitro benzo[a]pyrene diol epoxide‐induced DNA damage and chromosomal aberrations in primary lymphocytes, smoking, and risk of squamous cell carcinoma of the head and neck
Author(s) -
Xiong Ping,
Hu Zhibin,
Li Chunying,
Wang LiE,
ElNaggar Adel K.,
Sturgis Erich M.,
Wei Qingyi
Publication year - 2007
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.23054
Subject(s) - in vitro , head and neck cancer , epoxide , cancer research , head and neck , carcinogen , basal cell , pyrene , dna , dna damage , head and neck squamous cell carcinoma , pathology , medicine , biology , cancer , genetics , surgery , biochemistry , astrobiology , catalysis
Cigarette smoking is a major risk factor for squamous cell carcinoma of the head and neck (SCCHN), but only a fraction of those exposed to cigarette smoke develops SCCHN, suggesting variation in individual susceptibility. Tobacco smoke contains a number of carcinogens that cause various kinds of damage to DNA. In this study, we simultaneously measured benzo[a]pyrene diol epoxide‐induced DNA damage and chromosomal aberrations by the comet assay and the mutagen sensitivity assay, respectively, in cultured primary lymphocytes from newly recruited 123 patients with SCCHN and 136 age‐ and sex‐matched controls. Using the control median as the cut‐off, the elevated risk of SCCHN was 2.35 (95% CI, 1.37–4.03), 2.28 (95% CI, 1.34–3.98) and 3.25 (95% CI, 1.85–5.07) for high levels of tail extension, tail length and oliver tail moment of the comet assay, respectively, and 1.75 (95% CI, 1.04–2.94) for high levels of chromosomal aberrations of the mutagen sensitivity assay. The effects of these 2 types of measurements were additive; subjects with high levels of both DNA damage and chromosomal aberrations had a 4.77‐fold increased risk (95% CI, 2.73–8.36) of SCCHN. Cigarette smoking further elevated this risk to more than 20‐fold (OR 23.6; 95% CI, 8.92–62.3). These data support our previous finding that suboptimal repair contributed to susceptibility to SCCHN and the new data further suggests a possible gene‐environment interaction that may play an important role in the etiology of SCCHN. Further validation studies are warranted. © 2007 Wiley‐Liss, Inc.