Modification of Occupational Exposures on Bladder Cancer Risk by Common Genetic Polymorphisms
Few studies have demonstrated gene/environment interactions in cancer research. Using data on high-risk occupations for 2258 case patients and 2410 control patients from two bladder cancer studies, we observed that three of 16 known or candidate bladder cancer susceptibility variants displayed stati...
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creator | Figueroa, Jonine D Koutros, Stella Colt, Joanne S Kogevinas, Manolis Garcia-Closas, Montserrat Real, Francisco X Friesen, Melissa C Baris, Dalsu Stewart, Patricia Schwenn, Molly Johnson, Alison Karagas, Margaret R Armenti, Karla R Moore, Lee E Schned, Alan Lenz, Petra Prokunina-Olsson, Ludmila Banday, A Rouf Paquin, Ashley Ylaya, Kris Chung, Joon-Yong Hewitt, Stephen M Nickerson, Michael L Tardón, Adonina Serra, Consol Carrato, Alfredo García-Closas, Reina Lloreta, Josep Malats, Núria Fraumeni, Joseph F Chanock, Stephen J Chatterjee, Nilanjan Rothman, Nathaniel Silverman, Debra T |
description | Few studies have demonstrated gene/environment interactions in cancer research. Using data on high-risk occupations for 2258 case patients and 2410 control patients from two bladder cancer studies, we observed that three of 16 known or candidate bladder cancer susceptibility variants displayed statistically significant and consistent evidence of additive interactions; specifically, the GSTM1 deletion polymorphism (P ... ≤ .001), rs11892031 (UGT1A, P ... = .01), and rs798766 (TMEM129-TACC3-FGFR3, P ... = .03). There was limited evidence for multiplicative interactions. When we examined detailed data on a prevalent occupational exposure associated with increased bladder cancer risk, straight metalworking fluids, we also observed statistically significant additive interaction for rs798766 (TMEM129-TACC3-FGFR3, P ... = .02), with the interaction more apparent in patients with tumors positive for FGFR3 expression. All statistical tests were two-sided. The interaction we observed for rs798766 (TMEM129-TACC3-FGFR3) with specific exposure to straight metalworking fluids illustrates the value of integrating germline genetic variation, environmental exposures, and tumor marker data to provide insight into the mechanisms of bladder carcinogenesis. (ProQuest: ... denotes formulae/symbols omitted.) |
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Using data on high-risk occupations for 2258 case patients and 2410 control patients from two bladder cancer studies, we observed that three of 16 known or candidate bladder cancer susceptibility variants displayed statistically significant and consistent evidence of additive interactions; specifically, the GSTM1 deletion polymorphism (P ... ≤ .001), rs11892031 (UGT1A, P ... = .01), and rs798766 (TMEM129-TACC3-FGFR3, P ... = .03). There was limited evidence for multiplicative interactions. When we examined detailed data on a prevalent occupational exposure associated with increased bladder cancer risk, straight metalworking fluids, we also observed statistically significant additive interaction for rs798766 (TMEM129-TACC3-FGFR3, P ... = .02), with the interaction more apparent in patients with tumors positive for FGFR3 expression. All statistical tests were two-sided. The interaction we observed for rs798766 (TMEM129-TACC3-FGFR3) with specific exposure to straight metalworking fluids illustrates the value of integrating germline genetic variation, environmental exposures, and tumor marker data to provide insight into the mechanisms of bladder carcinogenesis. 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Using data on high-risk occupations for 2258 case patients and 2410 control patients from two bladder cancer studies, we observed that three of 16 known or candidate bladder cancer susceptibility variants displayed statistically significant and consistent evidence of additive interactions; specifically, the GSTM1 deletion polymorphism (P ... ≤ .001), rs11892031 (UGT1A, P ... = .01), and rs798766 (TMEM129-TACC3-FGFR3, P ... = .03). There was limited evidence for multiplicative interactions. When we examined detailed data on a prevalent occupational exposure associated with increased bladder cancer risk, straight metalworking fluids, we also observed statistically significant additive interaction for rs798766 (TMEM129-TACC3-FGFR3, P ... = .02), with the interaction more apparent in patients with tumors positive for FGFR3 expression. All statistical tests were two-sided. The interaction we observed for rs798766 (TMEM129-TACC3-FGFR3) with specific exposure to straight metalworking fluids illustrates the value of integrating germline genetic variation, environmental exposures, and tumor marker data to provide insight into the mechanisms of bladder carcinogenesis. 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Using data on high-risk occupations for 2258 case patients and 2410 control patients from two bladder cancer studies, we observed that three of 16 known or candidate bladder cancer susceptibility variants displayed statistically significant and consistent evidence of additive interactions; specifically, the GSTM1 deletion polymorphism (P ... ≤ .001), rs11892031 (UGT1A, P ... = .01), and rs798766 (TMEM129-TACC3-FGFR3, P ... = .03). There was limited evidence for multiplicative interactions. When we examined detailed data on a prevalent occupational exposure associated with increased bladder cancer risk, straight metalworking fluids, we also observed statistically significant additive interaction for rs798766 (TMEM129-TACC3-FGFR3, P ... = .02), with the interaction more apparent in patients with tumors positive for FGFR3 expression. All statistical tests were two-sided. The interaction we observed for rs798766 (TMEM129-TACC3-FGFR3) with specific exposure to straight metalworking fluids illustrates the value of integrating germline genetic variation, environmental exposures, and tumor marker data to provide insight into the mechanisms of bladder carcinogenesis. (ProQuest: ... denotes formulae/symbols omitted.)</abstract><cop>Oxford</cop><pub>Oxford Publishing Limited (England)</pub></addata></record> |
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subjects | Bladder cancer Gene expression Health risk assessment Occupational diseases Polymorphism |
title | Modification of Occupational Exposures on Bladder Cancer Risk by Common Genetic Polymorphisms |
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