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Pancreatic Neoplasms: HELP
Articles by Susan E. Steck
Based on 4 articles published since 2010
(Why 4 articles?)
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Between 2010 and 2020, Susan E. Steck wrote the following 4 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Dietary patterns and risk of pancreatic cancer: a systematic review. 2017

Zheng, Jiali / Guinter, Mark A / Merchant, Anwar T / Wirth, Michael D / Zhang, Jiajia / Stolzenberg-Solomon, Rachael Z / Steck, Susan E. ·Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, South Carolina, USA. · Cancer Prevention and Control Program, University of South Carolina, Columbia, South Carolina, USA. · Connecting Health Innovations LLC, Columbia, South Carolina, USA. · Division of Cancer Epidemiology and Genetics, Nutritional Epidemiology Branch, National Cancer Institute, Rockville, Maryland, USA. ·Nutr Rev · Pubmed #29025004.

ABSTRACT: Context: Pancreatic cancer has the highest case fatality rate of all major cancers. Objective: A systematic review using PRISMA guidelines was conducted to summarize the associations between dietary patterns and risk of pancreatic cancer. Data Sources: PubMed and Web of Science databases were searched for case-control and cohort studies published up to June 15, 2016. Study Selection: Eligible studies included a dietary pattern as exposure and pancreatic cancer incidence or mortality as outcome and reported odds ratios, hazard ratios, or relative risks, along with corresponding 95%CIs. Data Extraction: Important characteristics of each study, along with the dietary assessment instrument, the component foods or nutrients included in each dietary pattern or the scoring algorithm of a priori dietary patterns, were presented. For each dietary pattern identified, the estimate of association and the 95%CI comparing the highest versus the lowest category from the model with the most covariate adjustment were reported. Results: A total of 16 studies were identified. Among the 8 studies that examined data-driven dietary patterns, significant positive associations were found between pancreatic cancer risk and the Animal Products, Starch Rich, and Western dietary patterns, with effect estimates ranging from 1.69 to 2.40. Significant inverse relationships were found between risk of pancreatic cancer and dietary patterns designated as Fruits and Vegetables, Vitamins and Fiber, and Prudent, with effect estimates ranging from 0.51 to 0.55. Eight studies of a priori dietary patterns consistently suggested that improved dietary quality was associated with reduced risk of pancreatic cancer. Conclusions: Better diet quality is associated with reduced risk of pancreatic cancer. The associations between dietary patterns and pancreatic cancer were stronger in case-control studies than in cohort studies and were stronger among men than among women.

2 Article Pancreatic cancer risk is modulated by inflammatory potential of diet and ABO genotype: a consortia-based evaluation and replication study. 2018

Antwi, Samuel O / Bamlet, William R / Pedersen, Katrina S / Chaffee, Kari G / Risch, Harvey A / Shivappa, Nitin / Steck, Susan E / Anderson, Kristin E / Bracci, Paige M / Polesel, Jerry / Serraino, Diego / La Vecchia, Carlo / Bosetti, Cristina / Li, Donghui / Oberg, Ann L / Arslan, Alan A / Albanes, Demetrius / Duell, Eric J / Huybrechts, Inge / Amundadottir, Laufey T / Hoover, Robert / Mannisto, Satu / Chanock, Stephen J / Zheng, Wei / Shu, Xiao-Ou / Stepien, Magdalena / Canzian, Federico / Bueno-de-Mesquita, Bas / Quirós, José Ramon / Zeleniuch-Jacquotte, Anne / Bruinsma, Fiona / Milne, Roger L / Giles, Graham G / Hébert, James R / Stolzenberg-Solomon, Rachael Z / Petersen, Gloria M. ·Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. · Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. · Division of Oncology, Washington University, St. Louis, MO, USA. · Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT, USA. · Cancer Prevention and Control Program, USA. · Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA. · Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA. · Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA, USA. · Unit of Epidemiology and Biostatistics, Centro di Riferimento Oncologico, Aviano (PN), Italy. · Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy. · Department of Oncology, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. · Department of Gastrointestinal Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA. · Department of Environmental Medicine, New York University School of Medicine, New York, NY, USA. · Department of Population Health, New York University School of Medicine, New York, NY, USA. · Department of Obstetrics and Gynecology, New York University School of Medicine, New York, NY, USA. · Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA. · Unit of Nutrition and Cancer, Bellvitge Biomedical Research Institute-IDIBELL, Catalan Institute of Oncology-ICO. L'Hospitalet de Llobregat, Barcelona, Spain. · International Agency for Research on Cancer, World Health Organization, France. · Department of Public Health Solutions, National Institute for Health and Welfare Helsinki, Finland. · Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, and Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, TN, USA. · Genomic Epidemiology Group, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary's Campus, Norfolk Place, London, UK. · Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Pantai Valley, Kuala Lumpur, Malaysia. · Public Health Directorate, Asturias, Spain. · Perlmutter Cancer Center, New York University School of Medicine, New York, NY, USA. · Cancer Epidemiology and Intelligence Division, Cancer Council Victoria, and Centre for Epidemiology and Biostatistics, Melbourne School of Global and Population Health, The University of Melbourne, Melbourne, Australia. ·Carcinogenesis · Pubmed #29800239.

ABSTRACT: Diets with high inflammatory potential are suspected to increase risk for pancreatic cancer (PC). Using pooled analyses, we examined whether this association applies to populations from different geographic regions and population subgroups with varying risks for PC, including variation in ABO blood type. Data from six case-control studies (cases, n = 2414; controls, n = 4528) in the Pancreatic Cancer Case-Control Consortium (PanC4) were analyzed, followed by replication in five nested case-control studies (cases, n = 1268; controls, n = 4215) from the Pancreatic Cancer Cohort Consortium (PanScan). Two polymorphisms in the ABO locus (rs505922 and rs8176746) were used to infer participants' blood types. Dietary questionnaire-derived nutrient/food intake was used to compute energy-adjusted dietary inflammatory index (E-DII®) scores to assess inflammatory potential of diet. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable-adjusted logistic regression. Higher E-DII scores, reflecting greater inflammatory potential of diet, were associated with increased PC risk in PanC4 [ORQ5 versus Q1=2.20, 95% confidence interval (CI) = 1.85-2.61, Ptrend < 0.0001; ORcontinuous = 1.20, 95% CI = 1.17-1.24], and PanScan (ORQ5 versus Q1 = 1.23, 95% CI = 0.92-1.66, Ptrend = 0.008; ORcontinuous = 1.09, 95% CI = 1.02-1.15). As expected, genotype-derived non-O blood type was associated with increased PC risk in both the PanC4 and PanScan studies. Stratified analyses of associations between E-DII quintiles and PC by genotype-derived ABO blood type did not show interaction by blood type (Pinteraction = 0.10 in PanC4 and Pinteraction=0.13 in PanScan). The results show that consuming a pro-inflammatory diet and carrying non-O blood type are each individually, but not interactively, associated with increased PC risk.

3 Article Inflammatory potential of diet and risk of pancreatic cancer in the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial. 2018

Zheng, Jiali / Merchant, Anwar T / Wirth, Michael D / Zhang, Jiajia / Antwi, Samuel O / Shoaibi, Azza / Shivappa, Nitin / Stolzenberg-Solomon, Rachael Z / Hebert, James R / Steck, Susan E. ·Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC. · Cancer Prevention and Control Program, University of South Carolina, Columbia, SC. · Department of Epidemiology, Division of Cancer Prevention and Population Sciences, The University of Texas MD Anderson Cancer Center, Houston, TX. · Connecting Health Innovations, LLC, Columbia, SC. · Department of Health Sciences Research, Division of Epidemiology, Mayo Clinic, Jacksonville, FL. · Biomedical Informatics Center, Medical University of South Carolina, Charleston, SC. · Division of Cancer Epidemiology and Genetics, Metabolic Epidemiology Branch, National Cancer Institute (NCI/DCEG), Rockville, MD. ·Int J Cancer · Pubmed #29355939.

ABSTRACT: Inflammation plays a central role in pancreatic cancer etiology and can be modulated by diet. We aimed to examine the association between the inflammatory potential of diet, assessed with the Dietary Inflammatory Index (DII®), and pancreatic cancer risk in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial prospective cohort. Our study included 101,449 participants aged 52-78 years at baseline who completed both baseline questionnaire and a diet history questionnaire. Energy-adjusted DII (E-DII) scores were computed based on food and supplement intake. Cox proportional hazards models and time dependent Cox models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) with participants in the lowest E-DII quintile (most anti-inflammatory scores) as referent. After a median 8.5 years of follow-up, 328 pancreatic cancer cases were identified. E-DII scores were not associated with pancreatic cancer risk in the multivariable model (HR

4 Article Pancreatic cancer: associations of inflammatory potential of diet, cigarette smoking and long-standing diabetes. 2016

Antwi, Samuel O / Oberg, Ann L / Shivappa, Nitin / Bamlet, William R / Chaffee, Kari G / Steck, Susan E / Hébert, James R / Petersen, Gloria M. ·Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, 200 First Street SW, Charlton 6-243, Rochester, MN 55905, USA and. · Cancer Prevention and Control Program and Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC 29208, USA. ·Carcinogenesis · Pubmed #26905587.

ABSTRACT: Epidemiologic studies show strong associations between pancreatic cancer (PC) and inflammatory stimuli or conditions such as cigarette smoking and diabetes, suggesting that inflammation may play a key role in PC. Studies of dietary patterns and cancer outcomes also suggest that diet might influence an individual's risk of PC by modulating inflammation. We therefore examined independent and joint associations between inflammatory potential of diet, cigarette smoking and long-standing (≥5 years) type II diabetes in relation to risk of PC. Analyses included data from 817 cases and 1756 controls. Inflammatory potential of diet was measured using the dietary inflammatory index (DII), calculated from dietary intake assessed via a 144-item food frequency questionnaire, and adjusted for energy intake. Information on smoking and diabetes were obtained via risk factor questionnaires. Associations were examined using multivariable-adjusted logistic regression. Higher DII scores, reflecting a more proinflammatory diet, were associated with increased risk of PC [odds ratio (OR)Quintile 5 versus 1 = 2.54, 95% confidence interval (CI) = 1.87-3.46, P trend < 0.0001]. Excess risk of PC also was observed among former (OR = 1.29, 95% CI = 1.07-1.54) and current (OR = 3.40, 95% CI = 2.28-5.07) smokers compared with never smokers, and among participants with long-standing diabetes (OR = 3.09, 95% CI = 2.02-4.72) compared with nondiabetics. Joint associations were observed for the combined effects of having greater than median DII score, and being a current smoker (OR = 4.79, 95% CI = 3.00-7.65) or having long-standing diabetes (OR = 6.03, 95% CI = 3.41-10.85). These findings suggest that a proinflammatory diet may act as cofactor with cigarette smoking and diabetes to increase risk of PC beyond the risk of any of these factors alone.