SCCHN is the 5th most common cancer worldwide [9] with high mortality ratios among all malignancies accounting for 12% of all cancers in men and 8% of all cancers among women [10]. SCCHN are the commonest forms of cancers of the head and neck that start in the cells forming the lining of the mouth, nose, throat and ear or the surface covering the tongue. The major head and neck selleck products sites include the oral cavity, the pharynx (nasopharynx, oropharynx and hypopharynx),

the tongue (anterior 2/3rd and posterior 1/3rd or base of tongue), the larynx and the paranasal sinuses. Breast cancer is the primary subtype of cancer leading to death among women in developing countries.

13% out of the 58 million deaths worldwide in the year 2005 were caused due to cancer which included 502,000 deaths per year due to breast cancer. Well-established risk factors ascribed to breast cancer include early menarche, late menopause, age of first child’s birth, nulliparity and family history (FH) [11]. DNA repair is considered to play a key role in cancer susceptibility whereby some individuals are at very high risk of cancer due to SNPs in crucial DNA repair genes [12–15]. Inactivation or defect in DNA BI-D1870 ic50 repair genes may be associated with increased cancer risk [16]. Genetic polymorphisms in DNA repair genes are very common events [17–19], and some studies have shown a significant

effect of some of these polymorphisms in DNA repair capacity [20–22]. Evidence of inherited abnormalities in DNA repair genes and genes controlling carcinogen metabolism has been found to underline increase in risk of cancers [23]. The gene ERCC2 (located in the chromosomal location 19q13.3; OMIM ID 126340; Gene ID 2068; Gene length 18984) encodes the ERCC2/Xeroderma pigmentosum Type D (XPD) protein, which is one of the seven genetic complementation groups that forms an essential component of the Nucleotide excision repair (NER) pathway, a major DNA repair pathway that Paclitaxel removes photoproducts from UV radiation and bulky adducts from a huge number of chemicals, cross-links and oxidative damage through the action of 20 proteins and several multiprotein complexes [13, 24]. XPD is a highly VRT752271 polymorphic gene and correlation of its polymorphisms and cancer risk have been extensively studied [20, 25]. Among the genetic polymorphisms in ERCC2, the SNP causing amino acid change in codon 751 (Lys to Gln) (SNP ID rs13181) have been considered very important and there is evidence that subjects homozygous for the variant genotypes of XPD have suboptimal DNA repair capacity for benzo(a)pyrene adducts and UV DNA damage [26, 27].