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Your search keyword '"Ulrich C.M."' showing total 3 results
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3 results on '"Ulrich C.M."'

1. Mendelian randomization study of height and risk of colorectal cancer

Author

Thrift, A.P., Gong, J., Peters, U., Chang-Claude, J., Rudolph, A., Slattery, M.L., Chan, A.T., Esko, T., Wood, A.R., Yang, J., Vedantam, S., Gustafsson, S., Pers, T.H., GIANT Consortium (Albrecht, E., Gieger, C., Grallert, H., Heid, I.M., Illig, T., Müller-Nurasyid, M., Peters, A., Thorand, B., Wichmann, H.-E.), Baron, J.A., Bézieau, S., Kuery, S., Ogino, S., Berndt, S.I., Casey, G., Haile, R.W., Du, M., Harrison, T.A., Thornquist, M., Duggan, D.J., Le Marchand, L., Lemire, M., Lindor, N.M., Seminara, D., Song, M., Thibodeau, S.N., Cotterchio, M., Win, A.K., Jenkins, M.A., Hopper, J.L., Ulrich, C.M., Potter, J.D., Newcomb, P.A., Schoen, R.E., Hoffmeister, M., Brenner, H., White, E.S., Hsu, L.A., and Campbell, P.T.

Subjects
Male, Gerontology, medicine.medical_specialty, Mendelian Randomization Causal Analysis, Epidemiology, Logistic regression, Risk Factors, Mendelian randomization, Humans, Medicine, Sex Distribution, Body Height, Colorectal Cancer, Aged, Rectal Neoplasms, business.industry, Confounding, Case-control study, General Medicine, Odds ratio, Mendelian Randomization Analysis, Middle Aged, digestive system diseases, Confidence interval, Genetic epidemiology, Case-Control Studies, Colonic Neoplasms, Female, business, Demography
Abstract

Background: For men and women, taller height is associated with increased risk of all cancers combined. For colorectal cancer (CRC), it is unclear whether the differential association of height by sex is real or is due to confounding or bias inherent in observational studies. We performed a Mendelian randomization study to examine the association between height and CRC risk. Methods: To minimize confounding and bias, we derived a weighted genetic risk score predicting height (using 696 genetic variants associated with height) in 10 226 CRC cases and 10 286 controls. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI) for associations between height, genetically predicted height and CRC. Results: Using conventional methods, increased height (per 10-cm increment) was associated with increased CRC risk (OR = 1.08, 95% CI = 1.02–1.15). In sex-specific analyses, height was associated with CRC risk for women (OR = 1.15, 95% CI = 1.05–1.26), but not men (OR = 0.98, 95% CI = 0.92–1.05). Consistent with these results, carrying greater numbers of (weighted) height-increasing alleles (per 1-unit increase) was associated with higher CRC risk for women and men combined (OR = 1.07, 95% CI = 1.01–1.14) and for women (OR = 1.09, 95% CI = 1.01–1.19). There was weaker evidence of an association for men (OR = 1.05, 95% CI = 0.96–1.15). Conclusion: We provide evidence for a causal association between height and CRC for women. The CRC-height association for men remains unclear and warrants further investigation in other large studies.

Published
2015

2. A Review of the Application of Inflammatory Biomarkers in Epidemiologic Cancer Research

Author

Rayjean J. Hung, Darren R. Brenner, Paolo Boffetta, Cornelia M. Ulrich, Joellen M. Schildkraut, Ellen L. Goode, Margaret R. Spitz, Kenneth Muir, Dominique Scherer, Loic Le Marchand, Andrew T. Chan, Brenner, D.R., Scherer, D., Muir, K., Schildkraut, J., Boffetta, P., Spitz, M.R., Marchand, L.L., Chan, A.T., Goode, E.L., Ulrich, C.M., and Hung, R.J.

Subjects
Inflammation, Chemokine, Innate immune system, biology, Epidemiology, Angiogenesis, Cancer, medicine.disease, Inflammatory biomarkers, Article, Oncology, Neoplasms, Immunology, Biomarkers, Tumor, medicine, biology.protein, Humans, Inflammation Mediators, medicine.symptom, Epidemiologic Methods, multiple cancer types, Transcription factor, Cancer Etiology
Abstract

Inflammation is a facilitating process for multiple cancer types. It is believed to affect cancer development and progression through several etiologic pathways, including increased levels of DNA adduct formation, increased angiogenesis, and altered antiapoptotic signaling. This review highlights the application of inflammatory biomarkers in epidemiologic studies and discusses the various cellular mediators of inflammation characterizing the innate immune system response to infection and chronic insult from environmental factors. Included is a review of six classes of inflammation-related biomarkers: cytokines/chemokines, immune-related effectors, acute-phase proteins, reactive oxygen and nitrogen species, prostaglandins and cyclooxygenase-related factors, and mediators such as transcription factors and growth factors. For each of these biomarkers, we provide a brief overview of the etiologic role in the inflammation response and how they have been related to cancer etiology and progression within the literature. We provide a discussion of the common techniques available for quantification of each marker, including strengths, weaknesses, and potential pitfalls. Subsequently, we highlight a few under-studied measures to characterize the inflammatory response and their potential utility in epidemiologic studies of cancer. Finally, we suggest integrative methods for future studies to apply multifaceted approaches to examine the relationship between inflammatory markers and their roles in cancer development. Cancer Epidemiol Biomarkers Prev; 23(9); 1729–51. ©2014 AACR.

Published
2014

3. Cross Cancer Genomic Investigation of Inflammation Pathway for Five Common Cancers: Lung, Ovary, Prostate, Breast, and Colorectal Cancer

Author

Kenneth Muir, Christopher A. Haiman, S. Lindstrom, Nicholas Wentzensen, Ali A min Al Olama, Rosalind A. Eeles, Heike Bickeböller, Rayjean J. Hung, Loic L e Marchand, Stephen J. Chanock, Brooke L. Fridley, David C. Christiani, Christopher I. Amos, Brian E. Henderson, Peter Kraft, Richard S. Houlston, Zhihua Chen, P Brennan, David N. Rider, Ulrike Peters, Angela Risch, Graham Casey, Joellen M. Schildkraut, Andrew T. Chan, Paolo Boffetta, Catherine M. Phelan, John K. Field, Douglas F. Easton, Stephen B. Gruber, Julia G. Poirier, Cornelia M. Ulrich, Ellen L. Goode, Honglin Song, Sonja I. Berndt, John S. Witte, Fredrik Wiklund, Z Kote-Jarai, M. T. Landi, Henrik Grönberg, Fredrick R. Schumacher, Thomas A. Sellers, Yonathan Brhane, Margaret R. Spitz, David J. Hunter, Martha L. Slattery, Hung, R.J., Ulrich, C.M., Goode, E.L., Brhane, Y., Muir, K., Chan, A.T., Marchand, L.L., Schildkraut, J., Witte, J.S., Eeles, R., Boffetta, P., Spitz, M.R., Poirier, J.G., Rider, D.N., Fridley, B.L., Chen, Z., Haiman, C., Schumacher, F., Easton, D.F., Landi, M.T., Brennan, P., Houlston, R., Christiani, D.C., Field, J.K., Bickeböller, H., Risch, A., Kote-Jarai, Z., Wiklund, F., Grönberg, H., Chanock, S., Berndt, S.I., Kraft, P., Lindström, S., Al Olama, A.A., Song, H., Phelan, C., Wentzensen, N., Peters, U., Slattery, M.L., Sellers, T.A., Casey, G., Gruber, S.B., Hunter, D.J., Amos, C.I., and Henderson, B.

Subjects
Oncology, Male, Cancer Research, medicine.medical_specialty, Lung Neoplasms, Colorectal cancer, Genome-wide association study, Breast Neoplasms, Disease, Mouse model of colorectal and intestinal cancer, Biology, Article, Breast cancer, Prostate, Internal medicine, medicine, Humans, Lung cancer, Adaptor Proteins, Signal Transducing, Inflammation, Ovarian Neoplasms, Lung, ovary, prostate, breast, and colorectal cancer, Intracellular Signaling Peptides and Proteins, Prostatic Neoplasms, Proteins, medicine.disease, 3. Good health, medicine.anatomical_structure, Female, Ovarian cancer, Colorectal Neoplasms, Genome-Wide Association Study, Signal Transduction
Abstract

Background: Inflammation has been hypothesized to increase the risk of cancer development as an initiator or promoter, yet no large-scale study of inherited variation across cancer sites has been conducted. Methods: We conducted a cross-cancer genomic analysis for the inflammation pathway based on 48 genome-wide association studies within the National Cancer Institute GAME-ON Network across five common cancer sites, with a total of 64 591 cancer patients and 74 467 control patients. Subset-based meta-analysis was used to account for possible disease heterogeneity, and hierarchical modeling was employed to estimate the effect of the subcomponents within the inflammation pathway. The network was visualized by enrichment map. All statistical tests were two-sided. Results: We identified three pleiotropic loci within the inflammation pathway, including one novel locus in Ch12q24 encoding SH2B3 (rs3184504), which reached GWAS significance with a P value of 1.78 x 10-8, and it showed an association with lung cancer (P = 2.01 x 10-6), colorectal cancer (GECCO P = 6.72x10-6; CORECT P = 3.32x10-5), and breast cancer (P = .009). We also identified five key subpathway components with genetic variants that are relevant for the risk of these five cancer sites: inflammatory response for colorectal cancer (P = .006), inflammation related cell cycle gene for lung cancer (P = 1.35x10-6), and activation of immune response for ovarian cancer (P = .009). In addition, sequence variations in immune system development played a role in breast cancer etiology (P = .001) and innate immune response was involved in the risk of both colorectal (P = .022) and ovarian cancer (P = .003). Conclusions: Genetic variations in inflammation and its related subpathway components are keys to the development of lung, colorectal, ovary, and breast cancer, including SH2B3, which is associated with lung, colorectal, and breast cancer. © The Author 2015. Published by Oxford University Press. All rights reserved.

Published
2014

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