Susan E Steck1, Lesley M Butler2, Temitope Keku3, Samuel Antwi4, Joseph Galanko5, Robert S Sandler6, Jennifer J Hu7. 1. Department of Epidemiology and Biostatistics, Cancer Prevention and Control Program, Arnold School of Public Health, University of South Carolina, 915 Greene Street, RM 236, Columbia, SC 29208, USA. Electronic address: ssteck@sc.edu. 2. Cancer Control and Population Sciences, University of Pittsburgh Cancer Institute, UPMC Cancer Pavilion, Suite 4C-466, 5150 Centre Avenue, Pittsburgh, PA 15232, USA. Electronic address: BUTLERL3@upmc.edu. 3. Division of Gastroenterology and Hepatology, School of Medicine, University of North Carolina, 103 Mason Farm Road, 7340-C Medical Biomolecular Research Building, CB#7032, Chapel Hill, NC 27599-7032, USA. Electronic address: tokeku@med.unc.edu. 4. Department of Epidemiology and Biostatistics, Cancer Prevention and Control Program, Arnold School of Public Health, University of South Carolina, 915 Greene Street, RM 236, Columbia, SC 29208, USA. 5. Cancer Epidemiology Gastrointestinal Biology and Disease, School of Medicine, University of North Carolina at Chapel Hill, CB#7555, 4157 Bioinformatics Building, Chapel Hill, NC 27599-7555, USA. Electronic address: galanko@med.unc.edu. 6. Cancer Epidemiology Gastrointestinal Biology and Disease, School of Medicine, University of North Carolina at Chapel Hill, CB#7555, 4157 Bioinformatics Building, Chapel Hill, NC 27599-7555, USA. Electronic address: rsandler@med.unc.edu. 7. Sylvester Comprehensive Cancer Center and Department of Public Health Sciences, University of Miami Miller School of Medicine, Miami, FL, 33136, USA. Electronic address: JHu@med.miami.edu.
Abstract
PURPOSE: Much of the DNA damage from colon cancer-related carcinogens, including heterocyclic amines (HCA) and polycyclic aromatic hydrocarbons (PAH) from red meat cooked at high temperature, are repaired by the nucleotide excision repair (NER) pathway. Thus, we examined whether NER non-synonymous single nucleotide polymorphisms (nsSNPs) modified the association between red meat intake and colon cancer risk. METHODS: The study consists of 244 African-American and 311 white colon cancer cases and population-based controls (331 African Americans and 544 whites) recruited from 33 counties in North Carolina from 1996 to 2000. Information collected by food frequency questionnaire on meat intake and preparation methods were used to estimate HCA and benzo(a)pyrene (BaP, a PAH) intake. We tested 7 nsSNPs in 5 NER genes: XPC A499V and K939Q, XPD D312N and K751Q, XPF R415Q, XPG D1104H, and RAD23B A249V. Adjusted odds ratios (OR) and 95% confidence intervals (CI) were calculated using unconditional logistic regression. RESULTS: Among African Americans, we observed a statistically significant positive association between colon cancer risk and XPC 499 AV+VV genotype (OR=1.7, 95% CI: 1.1, 2.7, AA as referent), and an inverse association with XPC 939 QQ (OR=0.3, 95%CI: 0.2, 0.8, KK as referent). These associations were not observed among whites. For both races combined, there was interaction between the XPC 939 genotype, well-done red meat intake and colon cancer risk (OR=1.5, 95% CI=1.0, 2.2 for high well-done red meat and KK genotype as compared to low well-done red meat and KK genotype, pinteraction=0.05). CONCLUSIONS: Our data suggest that NER nsSNPs are associated with colon cancer risk and may modify the association between well-done red meat intake and colon cancer risk.
PURPOSE: Much of the DNA damage from colon cancer-related carcinogens, including heterocyclic amines (HCA) and polycyclic aromatic hydrocarbons (PAH) from red meat cooked at high temperature, are repaired by the nucleotide excision repair (NER) pathway. Thus, we examined whether NER non-synonymous single nucleotide polymorphisms (nsSNPs) modified the association between red meat intake and colon cancer risk. METHODS: The study consists of 244 African-American and 311 white colon cancer cases and population-based controls (331 African Americans and 544 whites) recruited from 33 counties in North Carolina from 1996 to 2000. Information collected by food frequency questionnaire on meat intake and preparation methods were used to estimate HCA and benzo(a)pyrene (BaP, a PAH) intake. We tested 7 nsSNPs in 5 NER genes: XPCA499V and K939Q, XPDD312N and K751Q, XPFR415Q, XPGD1104H, and RAD23BA249V. Adjusted odds ratios (OR) and 95% confidence intervals (CI) were calculated using unconditional logistic regression. RESULTS: Among African Americans, we observed a statistically significant positive association between colon cancer risk and XPC 499 AV+VV genotype (OR=1.7, 95% CI: 1.1, 2.7, AA as referent), and an inverse association with XPC 939 QQ (OR=0.3, 95%CI: 0.2, 0.8, KK as referent). These associations were not observed among whites. For both races combined, there was interaction between the XPC 939 genotype, well-done red meat intake and colon cancer risk (OR=1.5, 95% CI=1.0, 2.2 for high well-done red meat and KK genotype as compared to low well-done red meat and KK genotype, pinteraction=0.05). CONCLUSIONS: Our data suggest that NER nsSNPs are associated with colon cancer risk and may modify the association between well-done red meat intake and colon cancer risk.
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