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2. Corrigendum: genome-wide association study of colorectal cancer identifies six new susceptibility loci.

Author

Schumacher, Fredrick R, Schmit, Stephanie L, Jiao, Shuo, Edlund, Christopher K, Wang, Hansong, Zhang, Ben, Hsu, Li, Huang, Shu-Chen, Fischer, Christopher P, Harju, John F, Idos, Gregory E, Lejbkowicz, Flavio, Manion, Frank J, McDonnell, Kevin, McNeil, Caroline E, Melas, Marilena, Rennert, Hedy S, Shi, Wei, Thomas, Duncan C, Van Den Berg, David J, Hutter, Carolyn M, Aragaki, Aaron K, Butterbach, Katja, Caan, Bette J, Carlson, Christopher S, Chanock, Stephen J, Curtis, Keith R, Fuchs, Charles S, Gala, Manish, Giovannucci, Edward L, Gogarten, Stephanie M, Hayes, Richard B, Henderson, Brian, Hunter, David J, Jackson, Rebecca D, Kolonel, Laurence N, Kooperberg, Charles, Küry, Sébastien, LaCroix, Andrea, Laurie, Cathy C, Laurie, Cecelia A, Lemire, Mathieu, Levine, David, Ma, Jing, Makar, Karen W, Qu, Conghui, Taverna, Darin, Ulrich, Cornelia M, Wu, Kana, Kono, Suminori, West, Dee W, Berndt, Sonja I, Bezieau, Stephane, Brenner, Hermann, Campbell, Peter T, Chan, Andrew T, Chang-Claude, Jenny, Coetzee, Gerhard A, Conti, David V, Duggan, David, Figueiredo, Jane C, Fortini, Barbara K, Gallinger, Steven J, Gauderman, W James, Giles, Graham, Green, Roger, Haile, Robert, Harrison, Tabitha A, Hoffmeister, Michael, Hopper, John L, Hudson, Thomas J, Jacobs, Eric, Iwasaki, Motoki, Jee, Sun Ha, Jenkins, Mark, Jia, Wei-Hua, Joshi, Amit, Li, Li, Lindor, Noralene M, Matsuo, Keitaro, Moreno, Victor, Mukherjee, Bhramar, Newcomb, Polly A, Potter, John D, Raskin, Leon, Rennert, Gad, Rosse, Stephanie, Severi, Gianluca, Schoen, Robert E, Seminara, Daniela, Shu, Xiao-Ou, Slattery, Martha L, Tsugane, Shoichiro, White, Emily, Xiang, Yong-Bing, Zanke, Brent W, Zheng, Wei, Le Marchand, Loic, Casey, Graham, and Gruber, Stephen B

Subjects
MD Multidisciplinary
Published
2015

3. Folate‐mediated one‐carbon metabolism genes and interactions with nutritional factors on colorectal cancer risk: Women's Health Initiative Observational Study

Author

Cheng, Ting-Yuan David, Makar, Karen W, Neuhouser, Marian L, Miller, Joshua W, Song, Xiaoling, Brown, Elissa C, Beresford, Shirley AA, Zheng, Yingye, Poole, Elizabeth M, Galbraith, Rachel L, Duggan, David J, Habermann, Nina, Bailey, Lynn B, Maneval, David R, Caudill, Marie A, Toriola, Adetunji T, Green, Ralph, and Ulrich, Cornelia M

Subjects
Cancer, Digestive Diseases, Colo-Rectal Cancer, Nutrition, Genetics, Prevention, Aetiology, 2.1 Biological and endogenous factors, Aged, Biomarkers, Case-Control Studies, Colorectal Neoplasms, DNA-Binding Proteins, Female, Ferredoxin-NADP Reductase, Folic Acid, Genetic Predisposition to Disease, Histone-Lysine N-Methyltransferase, Humans, Logistic Models, Methylenetetrahydrofolate Dehydrogenase (NADP), Middle Aged, Minor Histocompatibility Antigens, Nuclear Proteins, Polymorphism, Single Nucleotide, Postmenopause, Risk Assessment, Transcription Factors, Vitamin B Complex, biomarker, colorectal cancer, gene-nutrient interaction, one-carbon metabolism, postmenopausal women, Oncology and Carcinogenesis, Public Health and Health Services, Oncology & Carcinogenesis
Abstract

BackgroundInvestigations of folate-mediated one-carbon metabolism (FOCM) genes and gene-nutrient interactions with respect to colorectal cancer (CRC) risk are limited to candidate polymorphisms and dietary folate. This study comprehensively investigated associations between genetic variants in FOCM and CRC risk and whether the FOCM nutrient status modified these associations.MethodsTwo hundred eighty-eight candidate and tagging single-nucleotide polymorphisms (SNPs) in 30 FOCM genes were genotyped for 821 incident CRC case-control matched pairs in the Women's Health Initiative Observational Study cohort. FOCM biomarkers (red blood cell [RBC] folate, plasma folate, pyridoxal-5'-phosphate [PLP], vitamin B12, and homocysteine) and self-reported alcohol consumption were measured at the baseline. Conditional logistic regression was implemented; effect modification was examined on the basis of known enzyme-nutrient relations.ResultsStatistically significant associations were observed between CRC risk and functionally defined candidate SNPs of methylenetetrahydrofolate dehydrogenase 1 (MTHFD1; K134R), 5-methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR; P450R), and PR domain containing 2 with ZNF domain (PRDM2; S450N) and a literature candidate SNP of thymidylate synthase (TYMS; g.676789A>T; nominal P

Published
2015

4. Erratum: Corrigendum: Genome-wide association study of colorectal cancer identifies six new susceptibility loci

Author

Schumacher, Fredrick R, Schmit, Stephanie L, Jiao, Shuo, Edlund, Christopher K, Wang, Hansong, Zhang, Ben, Hsu, Li, Huang, Shu-Chen, Fischer, Christopher P, Harju, John F, Idos, Gregory E, Lejbkowicz, Flavio, Manion, Frank J, McDonnell, Kevin, McNeil, Caroline E, Melas, Marilena, Rennert, Hedy S, Shi, Wei, Thomas, Duncan C, Van Den Berg, David J, Hutter, Carolyn M, Aragaki, Aaron K, Butterbach, Katja, Caan, Bette J, Carlson, Christopher S, Chanock, Stephen J, Curtis, Keith R, Fuchs, Charles S, Gala, Manish, Giovannucci, Edward L, Gogarten, Stephanie M, Hayes, Richard B, Henderson, Brian, Hunter, David J, Jackson, Rebecca D, Kolonel, Laurence N, Kooperberg, Charles, Küry, Sébastien, LaCroix, Andrea, Laurie, Cathy C, Laurie, Cecelia A, Lemire, Mathieu, Levine, David, Ma, Jing, Makar, Karen W, Qu, Conghui, Taverna, Darin, Ulrich, Cornelia M, Wu, Kana, Kono, Suminori, West, Dee W, Berndt, Sonja I, Bezieau, Stephane, Brenner, Hermann, Campbell, Peter T, Chan, Andrew T, Chang-Claude, Jenny, Coetzee, Gerhard A, Conti, David V, Duggan, David, Figueiredo, Jane C, Fortini, Barbara K, Gallinger, Steven J, Gauderman, W James, Giles, Graham, Green, Roger, Haile, Robert, Harrison, Tabitha A, Hoffmeister, Michael, Hopper, John L, Hudson, Thomas J, Jacobs, Eric, Iwasaki, Motoki, Jee, Sun Ha, Jenkins, Mark, Jia, Wei-Hua, Joshi, Amit, Li, Li, Lindor, Noralene M, Matsuo, Keitaro, Moreno, Victor, Mukherjee, Bhramar, Newcomb, Polly A, Potter, John D, Raskin, Leon, Rennert, Gad, Rosse, Stephanie, Severi, Gianluca, Schoen, Robert E, Seminara, Daniela, Shu, Xiao-Ou, Slattery, Martha L, Tsugane, Shoichiro, White, Emily, Xiang, Yong-Bing, Zanke, Brent W, Zheng, Wei, Le Marchand, Loic, Casey, Graham, and Gruber, Stephen B

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Digestive Diseases, Cancer, Colo-Rectal Cancer
Published
2015

5. Genome-wide association study of colorectal cancer identifies six new susceptibility loci.

Author

Schumacher, Fredrick R, Schmit, Stephanie L, Jiao, Shuo, Edlund, Christopher K, Wang, Hansong, Zhang, Ben, Hsu, Li, Huang, Shu-Chen, Fischer, Christopher P, Harju, John F, Idos, Gregory E, Lejbkowicz, Flavio, Manion, Frank J, McDonnell, Kevin, McNeil, Caroline E, Melas, Marilena, Rennert, Hedy S, Shi, Wei, Thomas, Duncan C, Van Den Berg, David J, Hutter, Carolyn M, Aragaki, Aaron K, Butterbach, Katja, Caan, Bette J, Carlson, Christopher S, Chanock, Stephen J, Curtis, Keith R, Fuchs, Charles S, Gala, Manish, Giovannucci, Edward L, Gogarten, Stephanie M, Hayes, Richard B, Henderson, Brian, Hunter, David J, Jackson, Rebecca D, Kolonel, Laurence N, Kooperberg, Charles, Küry, Sébastien, LaCroix, Andrea, Laurie, Cathy C, Laurie, Cecelia A, Lemire, Mathieu, Levine, David, Ma, Jing, Makar, Karen W, Qu, Conghui, Taverna, Darin, Ulrich, Cornelia M, Wu, Kana, Kono, Suminori, West, Dee W, Berndt, Sonja I, Bezieau, Stéphane, Brenner, Hermann, Campbell, Peter T, Chan, Andrew T, Chang-Claude, Jenny, Coetzee, Gerhard A, Conti, David V, Duggan, David, Figueiredo, Jane C, Fortini, Barbara K, Gallinger, Steven J, Gauderman, W James, Giles, Graham, Green, Roger, Haile, Robert, Harrison, Tabitha A, Hoffmeister, Michael, Hopper, John L, Hudson, Thomas J, Jacobs, Eric, Iwasaki, Motoki, Jee, Sun Ha, Jenkins, Mark, Jia, Wei-Hua, Joshi, Amit, Li, Li, Lindor, Noralene M, Matsuo, Keitaro, Moreno, Victor, Mukherjee, Bhramar, Newcomb, Polly A, Potter, John D, Raskin, Leon, Rennert, Gad, Rosse, Stephanie, Severi, Gianluca, Schoen, Robert E, Seminara, Daniela, Shu, Xiao-Ou, Slattery, Martha L, Tsugane, Shoichiro, White, Emily, Xiang, Yong-Bing, Zanke, Brent W, and Zheng, Wei

Subjects
Humans, Colorectal Neoplasms, Genetic Predisposition to Disease, Odds Ratio, Case-Control Studies, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Genetics, Digestive Diseases, Prevention, Cancer, Human Genome, Colo-Rectal Cancer, 2.1 Biological and endogenous factors, MD Multidisciplinary
Abstract

Genetic susceptibility to colorectal cancer is caused by rare pathogenic mutations and common genetic variants that contribute to familial risk. Here we report the results of a two-stage association study with 18,299 cases of colorectal cancer and 19,656 controls, with follow-up of the most statistically significant genetic loci in 4,725 cases and 9,969 controls from two Asian consortia. We describe six new susceptibility loci reaching a genome-wide threshold of P

Published
2015

6. Biomarkers of One-Carbon Metabolism Are Associated with Biomarkers of Inflammation in Women 1–3

Author

Abbenhardt, Clare, Miller, Joshua W, Song, Xiaoling, Brown, Elissa C, Cheng, Ting-Yuan David, Wener, Mark H, Zheng, Yingye, Toriola, Adetunji T, Neuhouser, Marian L, Beresford, Shirley AA, Makar, Karen W, Bailey, Lynn B, Maneval, David R, Green, Ralph, Manson, JoAnn E, Van Horn, Linda, and Ulrich, Cornelia M

Subjects
Prevention, Complementary and Integrative Health, Nutrition, Aetiology, 2.2 Factors relating to the physical environment, Aged, Biomarkers, C-Reactive Protein, Carbon, Chronic Disease, Cross-Sectional Studies, Cysteine, Erythrocytes, Female, Folic Acid, Homocysteine, Humans, Inflammation, Linear Models, Middle Aged, Nutritional Status, Risk Factors, Serum Amyloid A Protein, Vitamin B 12, Vitamin B 6, Animal Production, Food Sciences, Nutrition and Dietetics, Nutrition & Dietetics
Abstract

Folate-mediated one-carbon metabolism is essential for DNA synthesis, repair, and methylation. Perturbations in one-carbon metabolism have been implicated in increased risk of some cancers and may also affect inflammatory processes. We investigated these interrelated pathways to understand their relation. The objective was to explore associations between inflammation and biomarkers of nutritional status and one-carbon metabolism. In a cross-sectional study in 1976 women selected from the Women's Health Initiative Observational Study, plasma vitamin B-6 [pyridoxal-5'-phosphate (PLP)], plasma vitamin B-12, plasma folate, and RBC folate were measured as nutritional biomarkers; serum C-reactive protein (CRP) and serum amyloid A (SAA) were measured as biomarkers of inflammation; and homocysteine and cysteine were measured as integrated biomarkers of one-carbon metabolism. Student's t, chi-square, and Spearman rank correlations, along with multiple linear regressions, were used to explore relations between biomarkers; additionally, we tested stratification by folic acid fortification period and multivitamin use. With the use of univariate analysis, plasma PLP was the only nutritional biomarker that was modestly significantly correlated with serum CRP and SAA (ρ = -0.22 and -0.12, respectively; P < 0.0001). Homocysteine (μmol/L) showed significant inverse correlations with all nutritional biomarkers (ranging from ρ = -0.30 to ρ = -0.46; all P < 0.0001). With the use of multiple linear regression, plasma PLP, RBC folate, homocysteine, and cysteine were identified as independent predictors of CRP; and PLP, vitamin B-12, RBC folate, and homocysteine were identified as predictors of SAA. When stratified by folic acid fortification period, nutrition-homocysteine correlations were generally weaker in the postfortification period, whereas associations between plasma PLP and serum CRP increased. Biomarkers of inflammation are associated with PLP, RBC folate, and homocysteine in women. The connection between the pathways needs to be further investigated and causality established. The trial is registered at clinicaltrials.gov as NCT00000611.

Published
2014

7. Targeting innate immunity for tuberculosis vaccination

Author

Khader, Shabaana A., Divangahi, Maziar, Hanekom, Willem, Hill, Philip C., Maeurer, Markus, Makar, Karen W., Mayer-Barber, Katrin D., Mhlanga, Musa M., Nemes, Elisa, Schlesinger, Larry S., van Crevel, Reinout, Vankalayapati, Ramakrishna, Xavier, Ramnik J., Netea, Mihai G., and on behalf of the Bill and Melinda Gates Foundation Collaboration for TB Vaccine Discovery Innate Immunity Working Group

Subjects
Antigens -- Health aspects, Tuberculosis vaccines -- Health aspects, Epigenetic inheritance -- Health aspects, Lymphocytes -- Health aspects, BCG -- Health aspects, Antitubercular agents -- Health aspects, Medical research -- Health aspects, Vaccination -- Health aspects, Epidemiology -- Health aspects, Immune response -- Health aspects, Tuberculosis -- Development and progression -- Health aspects, Killer cells, T cells, B cells, Future predictions, Health care industry
Abstract

Vaccine development against tuberculosis (TB) is based on the induction of adaptive immune responses endowed with long-term memory against mycobacterial antigens. Memory B and T cells initiate a rapid and robust immune response upon encounter with Mycobacterium tuberculosis, thus achieving long-lasting protection against infection. Recent studies have shown, however, that innate immune cell populations such as myeloid cells and NK cells also undergo functional adaptation after infection or vaccination, a de facto innate immune memory that is also termed trained immunity. Experimental and epidemiological data have shown that induction of trained immunity contributes to the beneficial heterologous effects of vaccines such as bacille Calmette-Guerin (BCG), the licensed TB vaccine. Moreover, increasing evidence argues that trained immunity also contributes to the anti-TB effects of BCG vaccination. An interaction among immunological signals, metabolic rewiring, and epigenetic reprogramming underlies the molecular mechanisms mediating trained immunity in myeloid cells and their bone marrow progenitors. Future studies are warranted to explore the untapped potential of trained immunity to develop a future generation of TB vaccines that would combine innate and adaptive immune memory induction., Introduction Vaccination has made an enormous contribution to improving human and animal health over the last two centuries (1-6). Despite progress in developing vaccines against a large number of infections, [...]

Published
2019
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8. Identification of Genetic Susceptibility Loci for Colorectal Tumors in a Genome-Wide Meta-analysis

Author

Peters, Ulrike, Jiao, Shuo, Schumacher, Fredrick R, Hutter, Carolyn M, Aragaki, Aaron K, Baron, John A, Berndt, Sonja I, Bézieau, Stéphane, Brenner, Hermann, Butterbach, Katja, Caan, Bette J, Campbell, Peter T, Carlson, Christopher S, Casey, Graham, Chan, Andrew T, Chang–Claude, Jenny, Chanock, Stephen J, Chen, Lin S, Coetzee, Gerhard A, Coetzee, Simon G, Conti, David V, Curtis, Keith R, Duggan, David, Edwards, Todd, Fuchs, Charles S, Gallinger, Steven, Giovannucci, Edward L, Gogarten, Stephanie M, Gruber, Stephen B, Haile, Robert W, Harrison, Tabitha A, Hayes, Richard B, Henderson, Brian E, Hoffmeister, Michael, Hopper, John L, Hudson, Thomas J, Hunter, David J, Jackson, Rebecca D, Jee, Sun Ha, Jenkins, Mark A, Jia, Wei–Hua, Kolonel, Laurence N, Kooperberg, Charles, Küry, Sébastien, LaCroix, Andrea Z, Laurie, Cathy C, Laurie, Cecelia A, Le Marchand, Loic, Lemire, Mathieu, Levine, David, Lindor, Noralane M, Liu, Yan, Ma, Jing, Makar, Karen W, Matsuo, Keitaro, Newcomb, Polly A, Potter, John D, Prentice, Ross L, Qu, Conghui, Rohan, Thomas, Rosse, Stephanie A, Schoen, Robert E, Seminara, Daniela, Shrubsole, Martha, Shu, Xiao–Ou, Slattery, Martha L, Taverna, Darin, Thibodeau, Stephen N, Ulrich, Cornelia M, White, Emily, Xiang, Yongbing, Zanke, Brent W, Zeng, Yi–Xin, Zhang, Ben, Zheng, Wei, Hsu, Li, and Registry, Genetics and Epidemiology of Colorectal Cancer Consortium Colon Cancer Family

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Nutrition and Dietetics, Digestive Diseases, Prevention, Genetics, Cancer, Colo-Rectal Cancer, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Age Distribution, Aged, Aged, 80 and over, Colorectal Neoplasms, Cyclin D2, DNA-Binding Proteins, Female, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Incidence, Laminin, Male, Middle Aged, Polymorphism, Single Nucleotide, Prognosis, Risk Assessment, Sex Distribution, T-Box Domain Proteins, Colon Cancer Family Registry and the Genetics and Epidemiology of Colorectal Cancer Consortium, Neurosciences, Paediatrics and Reproductive Medicine, Gastroenterology & Hepatology, Clinical sciences, Nutrition and dietetics
Abstract

Background & aimsHeritable factors contribute to the development of colorectal cancer. Identifying the genetic loci associated with colorectal tumor formation could elucidate the mechanisms of pathogenesis.MethodsWe conducted a genome-wide association study that included 14 studies, 12,696 cases of colorectal tumors (11,870 cancer, 826 adenoma), and 15,113 controls of European descent. The 10 most statistically significant, previously unreported findings were followed up in 6 studies; these included 3056 colorectal tumor cases (2098 cancer, 958 adenoma) and 6658 controls of European and Asian descent.ResultsBased on the combined analysis, we identified a locus that reached the conventional genome-wide significance level at less than 5.0 × 10(-8): an intergenic region on chromosome 2q32.3, close to nucleic acid binding protein 1 (most significant single nucleotide polymorphism: rs11903757; odds ratio [OR], 1.15 per risk allele; P = 3.7 × 10(-8)). We also found evidence for 3 additional loci with P values less than 5.0 × 10(-7): a locus within the laminin gamma 1 gene on chromosome 1q25.3 (rs10911251; OR, 1.10 per risk allele; P = 9.5 × 10(-8)), a locus within the cyclin D2 gene on chromosome 12p13.32 (rs3217810 per risk allele; OR, 0.84; P = 5.9 × 10(-8)), and a locus in the T-box 3 gene on chromosome 12q24.21 (rs59336; OR, 0.91 per risk allele; P = 3.7 × 10(-7)).ConclusionsIn a large genome-wide association study, we associated polymorphisms close to nucleic acid binding protein 1 (which encodes a DNA-binding protein involved in DNA repair) with colorectal tumor risk. We also provided evidence for an association between colorectal tumor risk and polymorphisms in laminin gamma 1 (this is the second gene in the laminin family to be associated with colorectal cancers), cyclin D2 (which encodes for cyclin D2), and T-box 3 (which encodes a T-box transcription factor and is a target of Wnt signaling to β-catenin). The roles of these genes and their products in cancer pathogenesis warrant further investigation.

Published
2013

9. Meta-analysis of new genome-wide association studies of colorectal cancer risk

Author

Peters, Ulrike, Hutter, Carolyn M, Hsu, Li, Schumacher, Fredrick R, Conti, David V, Carlson, Christopher S, Edlund, Christopher K, Haile, Robert W, Gallinger, Steven, Zanke, Brent W, Lemire, Mathieu, Rangrej, Jagadish, Vijayaraghavan, Raakhee, Chan, Andrew T, Hazra, Aditi, Hunter, David J, Ma, Jing, Fuchs, Charles S, Giovannucci, Edward L, Kraft, Peter, Liu, Yan, Chen, Lin, Jiao, Shuo, Makar, Karen W, Taverna, Darin, Gruber, Stephen B, Rennert, Gad, Moreno, Victor, Ulrich, Cornelia M, Woods, Michael O, Green, Roger C, Parfrey, Patrick S, Prentice, Ross L, Kooperberg, Charles, Jackson, Rebecca D, LaCroix, Andrea Z, Caan, Bette J, Hayes, Richard B, Berndt, Sonja I, Chanock, Stephen J, Schoen, Robert E, Chang-Claude, Jenny, Hoffmeister, Michael, Brenner, Hermann, Frank, Bernd, Bézieau, Stéphane, Küry, Sébastien, Slattery, Martha L, Hopper, John L, Jenkins, Mark A, Le Marchand, Loic, Lindor, Noralane M, Newcomb, Polly A, Seminara, Daniela, Hudson, Thomas J, Duggan, David J, Potter, John D, and Casey, Graham

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Genetics, Colo-Rectal Cancer, Aging, Human Genome, Cancer, Prevention, Digestive Diseases, 2.1 Biological and endogenous factors, Aetiology, Colorectal Neoplasms, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Odds Ratio, Polymorphism, Single Nucleotide, Risk Factors, Complementary and Alternative Medicine, Paediatrics and Reproductive Medicine, Genetics & Heredity, Reproductive medicine
Abstract

Colorectal cancer is the second leading cause of cancer death in developed countries. Genome-wide association studies (GWAS) have successfully identified novel susceptibility loci for colorectal cancer. To follow up on these findings, and try to identify novel colorectal cancer susceptibility loci, we present results for GWAS of colorectal cancer (2,906 cases, 3,416 controls) that have not previously published main associations. Specifically, we calculated odds ratios and 95% confidence intervals using log-additive models for each study. In order to improve our power to detect novel colorectal cancer susceptibility loci, we performed a meta-analysis combining the results across studies. We selected the most statistically significant single nucleotide polymorphisms (SNPs) for replication using ten independent studies (8,161 cases and 9,101 controls). We again used a meta-analysis to summarize results for the replication studies alone, and for a combined analysis of GWAS and replication studies. We measured ten SNPs previously identified in colorectal cancer susceptibility loci and found eight to be associated with colorectal cancer (p value range 0.02 to 1.8 × 10(-8)). When we excluded studies that have previously published on these SNPs, five SNPs remained significant at p

Published
2012

10. Characterization of the association between 8q24 and colon cancer: gene-environment exploration and meta-analysis.

Author

Hutter, Carolyn M, Slattery, Martha L, Duggan, David J, Muehling, Jill, Curtin, Karen, Hsu, Li, Beresford, Shirley AA, Rajkovic, Aleksandar, Sarto, Gloria E, Marshall, James R, Hammad, Nazik, Wallace, Robert, Makar, Karen W, Prentice, Ross L, Caan, Bette J, Potter, John D, and Peters, Ulrike

Subjects
Chromosomes, Human, Pair 8, Humans, Colonic Neoplasms, Genetic Predisposition to Disease, Neoplasm Staging, Logistic Models, Odds Ratio, Risk Assessment, Risk Factors, Case-Control Studies, Life Style, Environment, Linkage Disequilibrium, Phenotype, Polymorphism, Single Nucleotide, Adult, Aged, Middle Aged, United States, Female, Male, Genetic Association Studies, Chromosomes, Human, Pair 8, Polymorphism, Single Nucleotide, Oncology and Carcinogenesis, Public Health and Health Services, Oncology & Carcinogenesis
Abstract

BackgroundGenome-wide association studies and subsequent replication studies have shown that single nucleotide polymorphisms (SNPs) in the chromosomal region 8q24 are associated with colorectal cancer susceptibility.MethodsWe examined 11 SNP markers in the 8q24 region between 128.47 and 128.54 Mb, using a total of 1,987 colon cases and 2,339 controls who self-reported as white from two independent, well-characterized study populations. Analysis was performed separately within each study, and combined using random effects meta-analysis. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs) and to test for effect modification by known colon cancer risk factors. We also performed a meta-analysis combining our results with previous studies.ResultsWe observed evidence of association for four SNPs in low to high linkage disequilibrium (r2 ranging from 0.18 to 0.93) localized in a 16.2 kb region defined by rs10505477 and rs1056368. The combined results for our two studies of colon cancer showed an OR of 1.10 (95% CI: 1.01-1.20, Ptrend = 0.023), and a meta-analysis of our results with previously reported studies of colon and colorectal cancer strongly support the association for this SNP (combined OR for rs6983267 = 1.21, 95% CI: 1.18-1.24, p = 5.5 × 10-44). We did not observe any notable evidence of effect modification by known colon cancer risk factors, and risk did not differ significantly by tumor site or stage.ConclusionsOur study confirms the association between polymorphisms on chromosome 8q24 and colon cancer risk and suggests that the susceptibility locus in region 8q24 is not strongly modified by various lifestyle, environmental, and demographic risk factors for colon cancer.

Published
2010

11. Data from Gene Expression Changes in Adipose Tissue with Diet- and/or Exercise-Induced Weight Loss

Author

Campbell, Kristin L., primary, Foster-Schubert, Karen E., primary, Makar, Karen W., primary, Kratz, Mario, primary, Hagman, Derek, primary, Schur, Ellen A., primary, Habermann, Nina, primary, Horton, Marc, primary, Abbenhardt, Clare, primary, Kuan, Ling-Yu, primary, Xiao, Liren, primary, Davison, Jerry, primary, Morgan, Martin, primary, Wang, Ching-Yun, primary, Duggan, Catherine, primary, McTiernan, Anne, primary, and Ulrich, Cornelia M., primary

Published
2023
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13. Supplementary Figure 2 from Gene Expression Changes in Adipose Tissue with Diet- and/or Exercise-Induced Weight Loss

Author

Campbell, Kristin L., primary, Foster-Schubert, Karen E., primary, Makar, Karen W., primary, Kratz, Mario, primary, Hagman, Derek, primary, Schur, Ellen A., primary, Habermann, Nina, primary, Horton, Marc, primary, Abbenhardt, Clare, primary, Kuan, Ling-Yu, primary, Xiao, Liren, primary, Davison, Jerry, primary, Morgan, Martin, primary, Wang, Ching-Yun, primary, Duggan, Catherine, primary, McTiernan, Anne, primary, and Ulrich, Cornelia M., primary

Published
2023
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15. Supplementary Tables from Gene Expression Changes in Adipose Tissue with Diet- and/or Exercise-Induced Weight Loss

Author

Campbell, Kristin L., primary, Foster-Schubert, Karen E., primary, Makar, Karen W., primary, Kratz, Mario, primary, Hagman, Derek, primary, Schur, Ellen A., primary, Habermann, Nina, primary, Horton, Marc, primary, Abbenhardt, Clare, primary, Kuan, Ling-Yu, primary, Xiao, Liren, primary, Davison, Jerry, primary, Morgan, Martin, primary, Wang, Ching-Yun, primary, Duggan, Catherine, primary, McTiernan, Anne, primary, and Ulrich, Cornelia M., primary

Published
2023
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16. Supplementary Figure Legends from Gene Expression Changes in Adipose Tissue with Diet- and/or Exercise-Induced Weight Loss

Author

Campbell, Kristin L., primary, Foster-Schubert, Karen E., primary, Makar, Karen W., primary, Kratz, Mario, primary, Hagman, Derek, primary, Schur, Ellen A., primary, Habermann, Nina, primary, Horton, Marc, primary, Abbenhardt, Clare, primary, Kuan, Ling-Yu, primary, Xiao, Liren, primary, Davison, Jerry, primary, Morgan, Martin, primary, Wang, Ching-Yun, primary, Duggan, Catherine, primary, McTiernan, Anne, primary, and Ulrich, Cornelia M., primary

Published
2023
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17. Supplementary Figure 1 from Gene Expression Changes in Adipose Tissue with Diet- and/or Exercise-Induced Weight Loss

Author

Campbell, Kristin L., primary, Foster-Schubert, Karen E., primary, Makar, Karen W., primary, Kratz, Mario, primary, Hagman, Derek, primary, Schur, Ellen A., primary, Habermann, Nina, primary, Horton, Marc, primary, Abbenhardt, Clare, primary, Kuan, Ling-Yu, primary, Xiao, Liren, primary, Davison, Jerry, primary, Morgan, Martin, primary, Wang, Ching-Yun, primary, Duggan, Catherine, primary, McTiernan, Anne, primary, and Ulrich, Cornelia M., primary

Published
2023
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20. Supplementary Table 2 from BRAF Mutation Status and Survival after Colorectal Cancer Diagnosis According to Patient and Tumor Characteristics

Author

Phipps, Amanda I., primary, Buchanan, Daniel D., primary, Makar, Karen W., primary, Burnett-Hartman, Andrea N., primary, Coghill, Anna E., primary, Passarelli, Michael N., primary, Baron, John A., primary, Ahnen, Dennis J., primary, Win, Aung Ko, primary, Potter, John D., primary, and Newcomb, Polly A., primary

Published
2023
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21. Supplementary Table 1 from BRAF Mutation Status and Survival after Colorectal Cancer Diagnosis According to Patient and Tumor Characteristics

Author

Phipps, Amanda I., primary, Buchanan, Daniel D., primary, Makar, Karen W., primary, Burnett-Hartman, Andrea N., primary, Coghill, Anna E., primary, Passarelli, Michael N., primary, Baron, John A., primary, Ahnen, Dennis J., primary, Win, Aung Ko, primary, Potter, John D., primary, and Newcomb, Polly A., primary

Published
2023
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23. Data from Vitamin D Related Genes, CYP24A1 and CYP27B1, and Colon Cancer Risk

Author

Dong, Linda M., primary, Ulrich, Cornelia M., primary, Hsu, Li, primary, Duggan, David J., primary, Benitez, Debbie S., primary, White, Emily, primary, Slattery, Martha L., primary, Farin, Fred M., primary, Makar, Karen W., primary, Carlson, Christopher S., primary, Caan, Bette J., primary, Potter, John D., primary, and Peters, Ulrike, primary

Published
2023
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38. Integrative post-genome-wide association analysis of CDKN2A and TP53 SNPs and risk of esophageal adenocarcinoma

Author

Buas, Matthew F., Levine, David M., Makar, Karen W., Utsugi, Heidi, Onstad, Lynn, Li, Xiaohong, Galipeau, Patricia C., Shaheen, Nicholas J., Hardie, Laura J., Romero, Yvonne, Bernstein, Leslie, Gammon, Marilie D., Casson, Alan G., Bird, Nigel C., Risch, Harvey A., Ye, Weimin, Liu, Geoffrey, Corley, Douglas A., Blount, Patricia L., Fitzgerald, Rebecca C., Whiteman, David C., Wu, Anna H., Reid, Brian J., and Vaughan, Thomas L.

Published
2014
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49. Characterization of the association between 8q24 and colon cancer: gene-environment exploration and meta-analysis

Author

Wallace Robert, Hammad Nazik, Marshall James R, Sarto Gloria E, Rajkovic Aleksandar, Beresford Shirley AA, Hsu Li, Curtin Karen, Muehling Jill, Duggan David J, Slattery Martha L, Hutter Carolyn M, Makar Karen W, Prentice Ross L, Caan Bette J, Potter John D, and Peters Ulrike

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Genome-wide association studies and subsequent replication studies have shown that single nucleotide polymorphisms (SNPs) in the chromosomal region 8q24 are associated with colorectal cancer susceptibility. Methods We examined 11 SNP markers in the 8q24 region between 128.47 and 128.54 Mb, using a total of 1,987 colon cases and 2,339 controls who self-reported as white from two independent, well-characterized study populations. Analysis was performed separately within each study, and combined using random effects meta-analysis. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs) and to test for effect modification by known colon cancer risk factors. We also performed a meta-analysis combining our results with previous studies. Results We observed evidence of association for four SNPs in low to high linkage disequilibrium (r2 ranging from 0.18 to 0.93) localized in a 16.2 kb region defined by rs10505477 and rs1056368. The combined results for our two studies of colon cancer showed an OR of 1.10 (95% CI: 1.01-1.20, Ptrend = 0.023), and a meta-analysis of our results with previously reported studies of colon and colorectal cancer strongly support the association for this SNP (combined OR for rs6983267 = 1.21, 95% CI: 1.18-1.24, p = 5.5 × 10-44). We did not observe any notable evidence of effect modification by known colon cancer risk factors, and risk did not differ significantly by tumor site or stage. Conclusions Our study confirms the association between polymorphisms on chromosome 8q24 and colon cancer risk and suggests that the susceptibility locus in region 8q24 is not strongly modified by various lifestyle, environmental, and demographic risk factors for colon cancer.

Published
2010
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50. Biomarkers of one-carbon metabolism are associated with biomarkers of inflammation in women

Author

Abbenhardt, Clare, Miller, Joshua W, Song, Xiaoling, Brown, Elissa C, Cheng, Ting-Yuan David, Wener, Mark H, Zheng, Yingye, Toriola, Adetunji T, Neuhouser, Marian L, Beresford, Shirley AA, Makar, Karen W, Bailey, Lynn B, Maneval, David R, Green, Ralph, Manson, Joann E, Van Horn, Linda, and Ulrich, Cornelia M

Subjects
Erythrocytes, Nutritional Status, Folic Acid, Food Sciences, Animal Production, Risk Factors, Complementary and Integrative Health, Humans, 2.2 Factors relating to the physical environment, Cysteine, Aetiology, Homocysteine, Aged, Nutrition, Inflammation, Serum Amyloid A Protein, Nutrition and Dietetics, Nutrition & Dietetics, Prevention, Middle Aged, Carbon, Vitamin B 6, Vitamin B 12, C-Reactive Protein, Cross-Sectional Studies, Chronic Disease, Linear Models, Female, Biomarkers
Abstract

Folate-mediated one-carbon metabolism is essential for DNA synthesis, repair, and methylation. Perturbations in one-carbon metabolism have been implicated in increased risk of some cancers and may also affect inflammatory processes. We investigated these interrelated pathways to understand their relation. The objective was to explore associations between inflammation and biomarkers of nutritional status and one-carbon metabolism. In a cross-sectional study in 1976 women selected from the Women's Health Initiative Observational Study, plasma vitamin B-6 [pyridoxal-5'-phosphate (PLP)], plasma vitamin B-12, plasma folate, and RBC folate were measured as nutritional biomarkers; serum C-reactive protein (CRP) and serum amyloid A (SAA) were measured as biomarkers of inflammation; and homocysteine and cysteine were measured as integrated biomarkers of one-carbon metabolism. Student's t, chi-square, and Spearman rank correlations, along with multiple linear regressions, were used to explore relations between biomarkers; additionally, we tested stratification by folic acid fortification period and multivitamin use. With the use of univariate analysis, plasma PLP was the only nutritional biomarker that was modestly significantly correlated with serum CRP and SAA (ρ = -0.22 and -0.12, respectively; P < 0.0001). Homocysteine (μmol/L) showed significant inverse correlations with all nutritional biomarkers (ranging from ρ = -0.30 to ρ = -0.46; all P < 0.0001). With the use of multiple linear regression, plasma PLP, RBC folate, homocysteine, and cysteine were identified as independent predictors of CRP; and PLP, vitamin B-12, RBC folate, and homocysteine were identified as predictors of SAA. When stratified by folic acid fortification period, nutrition-homocysteine correlations were generally weaker in the postfortification period, whereas associations between plasma PLP and serum CRP increased. Biomarkers of inflammation are associated with PLP, RBC folate, and homocysteine in women. The connection between the pathways needs to be further investigated and causality established. The trial is registered at clinicaltrials.gov as NCT00000611.

Published
2014

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