Publications
325 results found
Kabat GC, Cross AJ, Park Y, et al., 2009, Meat intake and meat preparation in relation to risk of postmenopausal breast cancer in the NIH-AARP diet and health study, INTERNATIONAL JOURNAL OF CANCER, Vol: 124, Pages: 2430-2435, ISSN: 0020-7136
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- Citations: 44
Murphy G, Cross AJ, Sansbury LS, et al., 2009, Dopamine D<sub>2</sub> receptor polymorphisms and adenoma recurrence in the Polyp Prevention Trial, INTERNATIONAL JOURNAL OF CANCER, Vol: 124, Pages: 2148-2151, ISSN: 0020-7136
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- Citations: 14
Ferrucci LM, Sinha R, Graubard BI, et al., 2009, Dietary Meat Intake in Relation to Colorectal Adenoma in Asymptomatic Women, AMERICAN JOURNAL OF GASTROENTEROLOGY, Vol: 104, Pages: 1231-1240, ISSN: 0002-9270
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- Citations: 50
Laiyemo AO, Pinsky PF, Marcus PM, et al., 2009, Utilization and Yield of Surveillance Colonoscopy in the Continued Follow-Up Study of the Polyp Prevention Trial, CLINICAL GASTROENTEROLOGY AND HEPATOLOGY, Vol: 7, Pages: 562-567, ISSN: 1542-3565
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- Citations: 97
Lam TK, Cross AJ, Consonni D, et al., 2009, Erratum: Article on red and processed meats, meat mutagens, and lung cancer (Cancer Res (2009) 69 (932:939)), Cancer Research, Vol: 69, ISSN: 0008-5472
Sinha R, Cross AJ, Graubard BI, et al., 2009, Meat Intake and Mortality <i>A Prospective Study of Over Half a Million People</i>, ARCHIVES OF INTERNAL MEDICINE, Vol: 169, Pages: 562-571, ISSN: 0003-9926
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- Citations: 370
Koutros S, Berndt SI, Sinha R, et al., 2009, Xenobiotic metabolizing gene variants, dietary heterocyclic amine intake, and risk of prostate cancer., Cancer Res, Vol: 69, Pages: 1877-1884
We recently reported that heterocyclic amines (HCA) are associated with prostate cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. We now use extensive genetic data from this resource to determine if risks associated with dietary HCAs {2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP); 2-amino-3,8-dimethylimidazo[4,5-b]quinoxaline (MeIQx); and 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx)} from cooked meat are modified by single nucleotide polymorphisms (SNP) in genes involved in HCA metabolism (CYP1A1, CYP1A2, CYP1B1, GSTA1, GSTM1, GSTM3, GSTP1, NAT1, NAT2, SULT1A1, SULT1A2, and UGT1A locus). We conducted a nested case-control study that included 1,126 prostate cancer cases and 1,127 controls selected for a genome-wide association study for prostate cancer. Unconditional logistic regression was used to estimate odds ratios (OR), 95% confidence intervals (95% CI), and P values for the interaction between SNPs, HCA intake, and risk of prostate cancer. The strongest evidence for an interaction was noted between DiMeIQx and MeIQx and the polymorphism rs11102001 downstream of the GSTM3 locus (P(interaction) = 0.001 for both HCAs; statistically significant after correction for multiple testing). Among men carrying the A variant, the risk of prostate cancer associated with high DiMeIQx intake was 2-fold greater than that with low intake (OR, 2.3; 95% CI, 1.2-4.7). The SNP rs11102001, which encodes a nonsynonymous amino acid change P356S in EPS8L3, is a potential candidate modifier of the effect of HCAs on prostate cancer risk. The observed effect provides evidence to support the hypothesis that HCAs may act as promoters of malignant transformation by altering mitogenic signaling.
Lam TK, Cross AJ, Consonni D, et al., 2009, Intakes of red meat, processed meat, and meat mutagens increase lung cancer risk., Cancer Res, Vol: 69, Pages: 932-939
Red and processed meat intake may increase lung cancer risk. However, the epidemiologic evidence is inconsistent and few studies have evaluated the role of meat mutagens formed during high cooking temperatures. We investigated the association of red meat, processed meat, and meat mutagen intake with lung cancer risk in Environment And Genetics in Lung cancer Etiology, a population-based case-control study. Primary lung cancer cases (n = 2,101) were recruited from 13 hospitals within the Lombardy region of Italy examining approximately 80% of the cases from the area. Noncancer population controls (n = 2,120), matched to cases on gender, residence, and age, were randomly selected from the same catchment area. Diet was assessed in 1,903 cases and 2,073 controls and used in conjunction with a meat mutagen database to estimate intake of heterocyclic amines (HCA) and benzo(a)pyrene (BaP). Multivariable odds ratios (OR) and 95% confidence intervals (95% CI) for sex-specific tertiles of intake were calculated using unconditional logistic regression. Red and processed meat were positively associated with lung cancer risk (highest-versus-lowest tertile: OR, 1.8; 95% CI, 1.5-2.2; P trend < 0.001 and OR, 1.7; 95% CI, 1.4-2.1; P trend < 0.001, respectively); the risks were strongest among never smokers (OR, 2.4; 95% CI, 1.4-4.0; P trend = 0.001 and OR, 2.5; 95% CI, 1.5-4.2; P trend = 0.001, respectively). HCAs and BaP were significantly associated with increased risk of lung cancer. When separated by histology, significant positive associations for both meat groups were restricted to adenocarcinoma and squamous cell carcinoma but not small cell carcinoma of the lung. In summary, red meat, processed meat, and meat mutagens were independently associated with increased risk of lung cancer.
Laiyemo AO, Murphy G, Sansbury LB, et al., 2009, Hyperplastic Polyps and the Risk of Adenoma Recurrence in the Polyp Prevention Trial, CLINICAL GASTROENTEROLOGY AND HEPATOLOGY, Vol: 7, Pages: 192-197, ISSN: 1542-3565
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- Citations: 40
Schatzkin A, Abnet CC, Cross AJ, et al., 2009, Mendelian Randomization: How It Can-and Cannot-Help Confirm Causal Relations between Nutrition and Cancer, CANCER PREVENTION RESEARCH, Vol: 2, Pages: 104-113, ISSN: 1940-6207
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- Citations: 51
Ferrucci LM, Cross AJ, Gunter MJ, et al., 2009, Xenobiotic Metabolizing Genes, Meat Intake, and Risk of Advanced Colorectal Adenoma, JOURNAL OF NUTRIGENETICS AND NUTRIGENOMICS, Vol: 2, Pages: 194-194, ISSN: 1661-6499
Morton LM, Wang SS, Cozen W, et al., 2008, Etiologic heterogeneity among non-Hodgkin lymphoma subtypes., Blood, Vol: 112, Pages: 5150-5160
Understanding patterns of etiologic commonality and heterogeneity for non-Hodgkin lymphomas may illuminate lymphomagenesis. We present the first systematic comparison of risks by lymphoma subtype for a broad range of putative risk factors in a population-based case-control study, including diffuse large B-cell (DLBCL; N = 416), follicular (N = 318), and marginal zone lymphomas (N = 106), and chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL; N = 133). We required at least 2 of 3 analyses to support differences in risk: (1) polytomous logistic regression, (2) homogeneity tests, or (3) dichotomous logistic regression, analyzing all 7 possible pairwise comparisons among the subtypes, corresponding to various groupings by clinical behavior, genetic features, and differentiation. Late birth order and high body mass index (>/= 35) kg/m(2)) increased risk for DLBCL alone. Autoimmune conditions increased risk for marginal zone lymphoma alone. The tumor necrosis factor G-308A polymorphism (rs1800629) increased risks for both DLBCL and marginal zone lymphoma. Exposure to certain dietary heterocyclic amines from meat consumption increased risk for CLL/SLL alone. We observed no significant risk factors for follicular lymphoma alone. These data clearly support both etiologic commonality and heterogeneity for lymphoma subtypes, suggesting that immune dysfunction is of greater etiologic importance for DLBCL and marginal zone lymphoma than for CLL/SLL and follicular lymphoma.
Cross AJ, Sinha R, 2008, Meat consumption and cancer, Pages: 272-281
The association between meat consumption and cancer risk has been studied extensively by a range of approaches, from highly controlled animal studies to large prospective epidemiologic studies. Many studies have reported an increased risk for colorectal cancer for those with a diet high in red or processed meat. Less definitive evidence suggests that high meat consumption may also increase the risk of a variety of other cancers, including some of the more prevalent cancers, such as breast and prostate cancers, as well as less common cancers, such as pancreatic, esophageal, and kidney cancers. There are several proposed mechanisms to support an association between meat and cancer, including preservation and processing procedures that can increase exposure to N-nitroso compounds. In addition, high-temperature cooking methods increase the formation of heterocyclic amines and polycyclic aromatic hydrocarbons, both of which are mutagenic. This article discusses the observational data and then elaborates on the mechanistic data relating meat intake to carcinogenesis. © 2008 Published by Elsevier Inc.
Cross AJ, Leitzmann MF, Subar AF, et al., 2008, A Prospective Study of Meat and Fat Intake in Relation to Small Intestinal Cancer, CANCER RESEARCH, Vol: 68, Pages: 9274-9279, ISSN: 0008-5472
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- Citations: 38
Schatzkin A, Park Y, Leitzmann MF, et al., 2008, Prospective study of dietary fiber, whole grain foods, and small intestinal cancer, GASTROENTEROLOGY, Vol: 135, Pages: 1163-1167, ISSN: 0016-5085
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- Citations: 77
Berndt SI, Potter JD, Hazra A, et al., 2008, Pooled analysis of genetic variation at chromosome 8q24 and colorectal neoplasia risk., Hum Mol Genet, Vol: 17, Pages: 2665-2672
Several different genetic variants at chromosome 8q24 have been related to prostate, breast and colorectal cancer risk with evidence of region-specific risk differentials for various tumor types. We investigated the association between 15 polymorphisms located in 8q24 regions associated with cancer risk in a pooled analysis of 2587 colorectal adenoma cases, 547 colorectal cancer cases and 2798 controls of European descent from four studies. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs) for the associations. Three polymorphisms (rs10808555, rs6983267 and rs7837328) located between 128.47 and 128.54 Mb were found to be associated with colorectal tumor risk. The association was strongest for the previously reported rs6983267 variant and was similar for both adenoma (OR(per allele) = 1.16, 95% CI: 1.07-1.25, P = 0.0002) and cancer (OR (per allele) = 1.17, 95% CI: 1.01-1.35, P = 0.03). The strength of the association of the regional haplotype containing variant alleles at rs10808555, rs6983267 and rs7837328 but not rs10505476 was greater than that of any single variant of both adenoma (OR = 1.27, P = 0.0001) and cancer (OR = 1.26, P = 0.03). The risk associated with rs6983267 was stronger for multiple adenomas (OR(per allele) = 1.29, P = 5.6 x 10(-6)) than for single adenoma (OR(per allele) = 1.10, P = 0.03) with P(heterogeneity) = 0.008. This study confirms the association between colorectal neoplasia and the 8q24 polymorphisms located between 128.47 and 128.54 Mb and suggests a role for these variants in the formation of multiple adenomas.
Murphy G, Sansbury LB, Cross AJ, et al., 2008, Folate and MTHFR: risk of adenoma recurrence in the Polyp Prevention Trial, CANCER CAUSES & CONTROL, Vol: 19, Pages: 751-758, ISSN: 0957-5243
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- Citations: 7
Ferrucci L, Flood A, Schatzkin A, et al., 2008, Meat, total iron, and heme iron intake in relation to colorectal adenoma in asymptomatic women, 41st Annual Meeting of the Society-for-Epidemiologic-Research, Publisher: OXFORD UNIV PRESS INC, Pages: S13-S13, ISSN: 0002-9262
Bobe G, Sansbury LB, Albert PS, et al., 2008, Dietary flavonoids and colorectal adenoma recurrence in the polyp prevention trial, CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION, Vol: 17, Pages: 1344-1353, ISSN: 1055-9965
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- Citations: 77
Laiyemo AO, Murphy GA, Sansbury LB, et al., 2008, Does the presence of synchronous hyperplastic polyps increase the risk of recurrent neoplasms among patients with colorectal adenomas?, Publisher: W B SAUNDERS CO-ELSEVIER INC, Pages: A186-A186, ISSN: 0016-5085
Laiyemo AO, Murphy G, Albert PS, et al., 2008, Postpolypectomy colonoscopy surveillance guidelines: Predictive accuracy for advanced adenorna at 4 years, ANNALS OF INTERNAL MEDICINE, Vol: 148, Pages: 419-426, ISSN: 0003-4819
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- Citations: 90
Cross AJ, Sinha R, Turesky RJ, 2008, Biomarkers for dietary carcinogens: the example of heterocyclic amines in epidemiologic studies, Molecular epidemiology of chronic diseases: new techniques and approaches, Editors: Wild, Publisher: Chichester, UK: John Wiley & Sons Ltd
Cross AJ, Sinha R, 2008, Meat and cooking-related carcinogens and colorectal cancer, Current challenges in the understanding and management of colon cancer, Editors: Nakagama, Dove, Mori, Wakabayashi, Publisher: Princess Takamatsu Cancer Research Fund
Lim U, Flood A, Choi S-W, et al., 2008, Genomic methylation of leukocyte DNA in relation to colorectal adenoma among asymptomatic women, GASTROENTEROLOGY, Vol: 134, Pages: 47-55, ISSN: 0016-5085
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- Citations: 84
Koutros S, Cross AJ, Sandler DP, et al., 2008, Meat and meat mutagens and risk of prostate cancer in the Agricultural Health Study., Cancer Epidemiol Biomarkers Prev, Vol: 17, Pages: 80-87, ISSN: 1055-9965
Meats cooked at high temperatures, such as pan-frying or grilling, are a source of carcinogenic heterocyclic amines and polycyclic aromatic hydrocarbons. We prospectively examined the association between meat types, meat cooking methods, meat doneness, and meat mutagens and the risk for prostate cancer in the Agricultural Health Study. We estimated relative risks and 95% confidence intervals (95% CI) for prostate cancer using Cox proportional hazards regression using age as the underlying time metric and adjusting for state of residence, race, smoking status, and family history of prostate cancer. During 197,017 person-years of follow-up, we observed 668 incident prostate cancer cases (613 of these were diagnosed after the first year of follow-up and 140 were advanced cases) among 23,080 men with complete dietary data. We found no association between meat type or specific cooking method and prostate cancer risk. However, intake of well or very well done total meat was associated with a 1.26-fold increased risk of incident prostate cancer (95% CI, 1.02-1.54) and a 1.97-fold increased risk of advanced disease (95% CI, 1.26-3.08) when the highest tertile was compared with the lowest. Risks for the two heterocyclic amines 2-amino-3,4,8-trimethylimidazo-[4,5-f]quinoxaline and 2-amino-3,8-dimethylimidazo-[4,5-b]quinoxaline were of borderline significance for incident disease [1.24 (95% CI, 0.96-1.59) and 1.20 (95% CI, 0.93-1.55), respectively] when the highest quintile was compared with the lowest. In conclusion, well and very well done meat was associated with an increased risk for prostate cancer in this cohort.
Stolzenberg-Solomon RZ, Cross AJ, Silverman DT, et al., 2007, Meat and meat-mutagen intake and pancreatic cancer risk in the NIH-AARP cohort, CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION, Vol: 16, Pages: 2664-2675, ISSN: 1055-9965
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- Citations: 93
Cross AJ, Leitzmann MF, Gail MH, et al., 2007, A prospective study of red and processed meat intake in relation to cancer risk, PLOS MEDICINE, Vol: 4, Pages: 1973-1984, ISSN: 1549-1277
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- Citations: 334
Hosgood HD, Baris D, Zahm SH, et al., 2007, Diet and risk of multiple myeloma in Connecticut women., Cancer Causes Control, Vol: 18, Pages: 1065-1076, ISSN: 0957-5243
Multiple myeloma accounts for an estimated 19,900 incident cancer cases per year in the United States. A population-based case-control study, consisting of 179 incident cases and 691 controls, was conducted to examine the impact of diet on multiple myeloma risk. Diet was assessed using a food frequency questionnaire and odds ratios, 95% confidence intervals, and P-trends were calculated across quartiles of consumption. After controlling for potential confounders, we observed inverse associations for cooked tomatoes (P-trend = 0.002), cruciferous vegetables (P-trend = 0.01), fresh fish (P-trend < 0.001), alcohol (P-trend < 0.001), and vitamin A (P-trend < 0.001) with multiple myeloma risk. In contrast, consumption of cream soups (P-trend = 0.01), jello (P-trend = 0.01), ice cream (P-trend = 0.01), and pudding (P-trend < 0.001) were positively associated with multiple myeloma. Furthermore, there was a suggestion that carbohydrate intake may be positively associated, whereas vitamin D and calcium intake may be inversely associated, with multiple myeloma risk. Despite very limited data on dietary factors in relation to multiple myeloma, the findings from this study concur with previously published studies, suggesting an inverse association for consumption of fish, cruciferous vegetables and green vegetables, and a positive association for some dairy products.
Lee WJ, Sandler DP, Blair A, et al., 2007, Pesticide use and colorectal cancer risk in the Agricultural Health Study., Int J Cancer, Vol: 121, Pages: 339-346, ISSN: 0020-7136
We investigated the relationship between agricultural pesticides and colorectal cancer incidence in the Agricultural Health Study. A total of 56,813 pesticide applicators with no prior history of colorectal cancer were included in this analysis. Detailed pesticide exposure and other information were obtained from self-administered questionnaires completed at the time of enrollment (1993-1997). Cancer incidence was determined through population-based cancer registries from enrollment through December 31, 2002. A total of 305 incident colorectal cancers (212 colon, 93 rectum) were diagnosed during the study period, 1993-2002. Although most of the 50 pesticides studied were not associated with colorectal cancer risk, chlorpyrifos use showed significant exposure response trend (p for trend = 0.008) for rectal cancer, rising to a 2.7-fold (95% confidence interval: 1.2-6.4) increased risk in the highest exposure category. Aldicarb was associated with a significantly increased risk of colon cancer (p for trend = 0.001), based on a small number of exposed cases, with the highest exposure category resulting in a 4.1-fold increased risk (95% confidence interval: 1.3-12.8). In contrast, dichlorophenoxyacetic acid showed a significant inverse association with colon cancer but the association was not monotonic. Our findings should be interpreted cautiously since the literature suggesting that pesticides are related to colorectal cancer is limited. Nonetheless the possibility of an association between exposure to certain pesticides and incidence of colorectal cancer among pesticide applicators deserves further evaluation.
Ward MH, Cross AJ, Divan H, et al., 2007, Processed meat intake, CYP2A6 activity and risk of colorectal adenoma., Carcinogenesis, Vol: 28, Pages: 1210-1216, ISSN: 0143-3334
Red and processed meat intake is associated with increased risks of both colorectal adenoma and cancer. Processed meats contain nitrate and nitrite, precursors of N-nitroso compounds (NOCs); furthermore, meats cooked at high temperatures contain heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs). Specific NOC, HCA and PAH are mutagens and animal carcinogens. We conducted a case-control study of 146 cases of colorectal adenoma, diagnosed at sigmoidoscopy or colonoscopy, and 228 polyp-free controls. We calculated odds ratios (ORs) [and 95% confidence intervals (CIs)] and found a 2-fold increased risk in the highest, compared with the lowest, quartile of processed meat intake (95% CI = 1.0-4.0). We estimated nitrate and nitrite intake from meat using published data from the literature as well as from actual measurements of meats analyzed recently. We evaluated the interaction of processed meat and nitrate plus nitrite intake with CYP2A6 activity, an enzyme able to metabolize some NOC to their carcinogenic form. Results for both methods of estimating nitrate and nitrite intake were similar; compared with the lowest, the highest quartile based on measured values was associated with a 2-fold elevated risk (95% CI = 1.0-3.9). Adjustment for the HCA 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) attenuated the association (OR = 1.6, 95% CI = 0.8-3.2), but other HCA and PAH had minimal effect. Higher CYP2A6 activity was not associated with risk and there was no evidence of an interaction of CYP2A6 activity with nitrate and nitrite intake. Our results suggest that nitrite and nitrate intake from processed meat intake increases the risk of colorectal adenoma after accounting for HCA and PAH.
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