A Population-Based Case-Control Study of the <i>XRCC1</i> <i>Arg399Gln</i> Polymorphism and Susceptibility to Bladder Cancer

Kelsey, Karl T.; Park, Sunyeong; Nelson, Heather H.; Karagas, Margaret R.

doi:10.1158/1055-9965.1337.13.8

Cited by 48 publications

References 13 publications

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Smoking modifies the relationship between XRCC1 haplotypes and HPV16‐negative head and neck squamous cell carcinoma

Applebaum

McClean

Nelson

et al. 2009

Intl Journal of Cancer

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Reports on the relationship between head and neck squamous cell carcinoma (HNSCC) and polymorphisms in X-ray cross complementing group 1 (XRCC1) have been inconsistent. We hypothesized this may be due to not accounting for Human papillomavirus type-16 (HPV16) and thus examined whether smoking modified the association between XRCC1 haplotypes and HNSCC risk within HPV16 serologic strata. Cases were diagnosed in Greater Boston, Massachusetts. Controls were matched to cases on age, gender and residential town. Genotyping was conducted on three XRCC1 polymorphisms (Arg194Trp, Arg280His and Arg399Gln) and serology was used to determine HPV16 exposure. Unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs), adjusting for age, sex, race, education, smoking, alcohol consumption and HPV16 serology. There was no overall association between XRCC1 polymorphisms and HNSCC risk. Smoking did not modify the association between XRCC1 polymorphisms and HNSCC risk among the HPV16 seropositive (p interaction 5 0.89) but it did for the HPV16 seronegative (p interaction 50.04). Among the HPV16 seronegative, heavy smokers with a haplotype containing a variant allele had an increased HNSCC risk (haplotype with 399Gln: OR, 1.35; 95% CI, 0.97-1.86), whereas never/light smokers with variant alleles may have a reduced risk. In sum, the association between XRCC1 and HNSCC risk differed by HPV16 status and smoking. Among the HPV16 seronegative, heavy smokers with XRCC1 variant alleles had an increased HNSCC risk. There was no relationship between XRCC1 and HPV16-related HNSCC, regardless of smoking. Our findings underscore the importance of accounting for HPV16 exposure even when studying susceptibility to HNSCC. ' 2009 Wiley-Liss, Inc.Key words: Human papillomavirus (HPV); head and neck squamous cell carcinoma (HNSCC); tobacco; XRCC1; DNA repair Approximately 434,000 new cases of head and neck squamous cell carcinoma (HNSCC) are expected worldwide annually 1 and over 45,000 of these will occur in the U.S.2 Tobacco and alcohol together are thought to explain 75% of HNSCC incidence.3 The predominant risk factor, tobacco, contains numerous known carcinogens including benzene, polycyclic aromatic hydrocarbons and nitrosamines. A review of the literature found that smokers are at a 3-to 12-fold greater risk of HNSCC than nonsmokers and among those who do not drink alcohol, the relative risks for smoking were between 2 and 5.

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Smoking modifies the relationship between XRCC1 haplotypes and HPV16‐negative head and neck squamous cell carcinoma

Applebaum

McClean

Nelson

et al. 2009

Intl Journal of Cancer

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Genetic and epigenetic aspects of bladder cancer

Kim

Quan

2005

J of Cellular Biochemistry

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Transitional cell carcinoma of the urinary bladder has a diverse collection of biologic and functional characteristics. This is reflected in differing clinical courses. The diagnosis of bladder cancer is based on the information provided by cystoscopy, the gold standard in combination with urinary cytology findings. Many tumor markers have been evaluated for detecting and monitoring the disease in serum, bladder washes, and urinary specimens. However, none of these biomarkers reported to date has shown sufficient sensitivity and specificity for the detection of the whole spectrum of bladder cancer diseases in routine clinical practice. The limited value of established prognostic markers requires the analysis of new molecular parameters of interest in predicting the prognosis of bladder cancer patients; in particular, the high-risk patient groups at risk of progression and recurrence. Over the past decade, there has been major progress elucidating of the molecular genetic and epigenetic changes leading to the development of transitional cell carcinoma. This review focuses on the recent advances of genetic and epigenetic aspects in bladder cancer, and emphasizes how molecular biology would be likely to affect the future therapies.

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Cigarette Smoke and Oxidative DNA Modification

Poulsen

Weimann

Halliwell

Cigarette Smoke and Oxidative Stress

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A Population-Based Case-Control Study of the XRCC1 Arg399Gln Polymorphism and Susceptibility to Bladder Cancer

Cited by 48 publications

References 13 publications

Smoking modifies the relationship between XRCC1 haplotypes and HPV16‐negative head and neck squamous cell carcinoma

Smoking modifies the relationship between XRCC1 haplotypes and HPV16‐negative head and neck squamous cell carcinoma

Genetic and epigenetic aspects of bladder cancer

Cigarette Smoke and Oxidative DNA Modification

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