%0 Journal Article
%T Variation in HNF1B and Obesity May Influence Prostate Cancer Risk in African American Men: A Pilot Study
%A Ganna Chornokur
%A Ernest K. Amankwah
%A Stacy N. Davis
%A Catherine M. Phelan
%A Jong Y. Park
%A Julio Pow-Sang
%A Nagi B. Kumar
%J Prostate Cancer
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/384594
%X Background. Prostate cancer (PCa) racial disparity is multifactorial, involving biological, sociocultural, and lifestyle determinants. We investigated the association between selected potentially functional polymorphisms (SNPs) and prostate cancer (PCa) risk in Black (AAM) and White (EAM) men. We further explored if these associations varied by the body mass index (BMI) and height. Methods. Age-matched DNA samples from 259 AAM and 269 EAM were genotyped for 10 candidate SNPs in 7 genes using the TaqMan allelic differentiation analysis. The dominant, recessive, and additive age-adjusted unconditional logistic regression models were fitted. Results. Three SNPs showed statistically significant associations with PCa risk: in AAM, HNF1B rs7501939 ( , ) and rs4430796 ( , ); in EAM, CTBP2 rs4962416 ( , ). In addition, high BMI in AAM ( , ) and height in EAM ( , ) showed significant associations. Interestingly, HNF1B rs7501939 was associated with PCa exclusively in obese AAM ( , ). Conclusion. Our results suggest that variation in the HNF1B may influence PCa risk in obese AAM. 1. Introduction Prostate cancer (PCa) remains the most common type of solid malignancy and the second-leading cause of all cancer death in US men [1]. However, the burden of PCa is not the same across all racial and ethnic groups, as African American/Black men (AAM) consistently demonstrate 1.6 times higher incidence and 2-3 times higher mortality rates of PCa, compared to their nonhispanic white (EAM) counterparts [2]. In addition, AAM are more likely to be diagnosed at an earlier age and have more aggressive tumors and higher recurrence rates following definite treatments [2, 3]. The etiology of racial disparity in PCa is thought to be multifactorial, involving biological, sociocultural, and lifestyle determinants [4]. Although genome-wide association studies (GWAS) have identified more than a dozen PCa risk loci [5], elucidating the biological basis for these associations is challenging [6]. Identified risk loci include the noncoding variants, such as those located in the 8q24 region [7], as well as polymorphisms in the coding regions (genes) that either alter, or are predicted to alter, the protein expression (such as HNF1B [8], TERT [5], and RNASEL [9]). The post-GWAS studies are increasingly suggestive of the interaction between genetic variants and environmental risk factors [10] for which our understanding is still largely inadequate [11]. Established risk factors for PCa are increasing age, race, and family history of the disease [2¨C4]. Obesity (which affects 35% of all US adults
%U http://www.hindawi.com/journals/pc/2013/384594/