Recently, Sreeja at al (2008) has shown that the carriers of XRCC1 Gln399Gln genotypes INCB028050 chemical structure were at higher risk of lung cancer [12]. On the other hand, López-Cima et al. (2007) has been reported that individuals homozygous for the XRCC1 Gln339 allele presented no risk of developing lung cancer [6]. The association between XRCC1 Arg399Gln polymorphism and ductal carcinoma

of women with breast cancer was found statistically significant in studies performed by Dufloth et al. at 2008 [13]. Despite of large number of studies, in well-characterized populations, results from HNSCC patients are still confusing. There was a marginally significant risk of HNSCC observed in variants of XRCC1 genotype with Trp194 allele in Thailand population [41]. No altered SN-38 clinical trial risk was associated with the XRCC1 Arg399Gln genotype in Li et al. studies [42], however smokers carrying risk genotype of XRCC1 with dominant Gln399 allele were over-represented in head and neck cancer populations from eastern region of India [43]. Recently, combinational polymorphisms of four DNA Selleckchem MK-4827 Repair genes XRCC1, XRCC2, XRCC3, and XRCC4 and their association with HNSCC cancer in Taiwan has been investigated. [14]. Except for XRCC2, none of SNPs was found to individually contribute to cancer risk. In our study, we found that Gln399 allele may also increase head and neck cancer risk in population with positive smoking status.

Finally, no association was found individually for either analyzed SNPs but we evidenced that combined genotypes of XRCC1 may have impact on HNSCC risk. Conclusion Head and neck cancer patients have variable prognoses even within the same clinical stage and while receiving similar treatments. The number of studies of genetic polymorphisms as prognostic factors of HNSCC outcomes is growing. Candidate polymorphisms have been evaluated in DNA repair, cell cycle, xenobiotic metabolism, and growth factor pathways. In our study, we assessed two common polymorphisms of the XRCC1 gene that might influence DNA repair capacity and their association with head and neck cancer risk. Finally, we identified the combined

genotype of Arg194Trp-Arg399Arg that was associated with HNSCC cancer risk and may have an impact on identification Sitaxentan of a high-risk population. Acknowledgements This work was supported by grant N301 099 32/3581 from Polish Ministry of Science and Higher Education. References 1. Lindahl T, Wood RD: Quality control by DNA repair. Science 1999, 286: 1897–1905.CrossRefPubMed 2. Hoeijmakers JH: Genome maintenance mechanisms for preventing cancer. Nature 2001, 411: 366–374.CrossRefPubMed 3. Barnes DE, Lindahl T: Repair and genetic consequences of endogenous DNA base damage in mammalian cells. Annu Rev Genet 2004, 38: 445–476.CrossRefPubMed 4. Vogelstein B, Kinzler KW: Cancer genes and the pathways they control. Nat Med 2004, 10: 789–799.CrossRefPubMed 5.