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Pancreatic Neoplasms: HELP
Articles by Anna E. Prizment
Based on 7 articles published since 2010
(Why 7 articles?)
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Between 2010 and 2020, A. Prizment wrote the following 7 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Soluble MICA is elevated in pancreatic cancer: Results from a population based case-control study. 2017

Onyeaghala, Guillaume / Nelson, Heather H / Thyagarajan, Bharat / Linabery, Amy M / Panoskaltsis-Mortari, Angela / Gross, Myron / Anderson, Kristin E / Prizment, Anna E. ·Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota. · University of Minnesota Masonic Cancer Center, Minneapolis, Minnesota. · Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota. · Division of Blood and Marrow Transplantation, Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota. ·Mol Carcinog · Pubmed #28470829.

ABSTRACT: Pancreatic cancer is diagnosed at a late stage and has one of the highest cancer mortality rates in the United States, creating an urgent need for novel early detection tools. A candidate biomarker for use in early detection is the soluble MHC class I-related chain A (s-MICA) ligand, which pancreatic tumors shed to escape immune detection. The objective of this study was to define the association between s-MICA levels and pancreatic cancer, in a population-based case-control study. S-MICA was measured in 143 pancreatic cancer cases and 459 controls. Unconditional logistic regression was used to calculate odds ratio (OR) for pancreatic cancer and 95% confidence intervals (CI). There was a positive association between increasing s-MICA levels and pancreatic cancer: compared to the lowest tertile, the ORs for pancreatic cancer were 1.25 (95%CI: 0.75-2.07) and 2.10 (95%CI: 1.29-3.42) in the second and highest tertiles, respectively (P-trend = 0.02). Our study supports previous work demonstrating a positive association between plasma s-MICA levels and pancreatic cancer.

2 Article Aspirin use and the incidence of breast, colon, ovarian, and pancreatic cancers in elderly women in the Iowa Women's Health Study. 2016

Vaughan, Lisa E / Prizment, Anna / Blair, Cindy K / Thomas, William / Anderson, Kristin E. ·Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, MN, USA. · Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, 1300 S. 2nd Street Suite 300, Minneapolis, MN, USA. · Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA. · Department of Internal Medicine, University of New Mexico, Albuquerque, NM, USA. · University of New Mexico Comprehensive Cancer Center, Albuquerque, NM, USA. · Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, 1300 S. 2nd Street Suite 300, Minneapolis, MN, USA. ander116@umn.edu. · Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA. ander116@umn.edu. ·Cancer Causes Control · Pubmed #27677628.

ABSTRACT: PURPOSE: Few studies have evaluated the chemopreventive effect of aspirin on the cancer risk in elderly women. We examined associations between frequency, dose, and duration of aspirin use with incidence of 719 aspirin-sensitive cancers (cancers of colon, pancreas, breast, and ovaries) in the Iowa Women's Health Study (IWHS), a prospective cohort of women over 70 years old. METHODS: Aspirin frequency, dose, and duration were self-reported in the 2004 IWHS questionnaire. Women were followed-up to 2011. Cancer cases were ascertained by linkage to the Iowa State Health Registry. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95 % confidence intervals (CI). RESULTS: Among the 14,386 women, 30 % were nonusers of aspirin; 34 % used low-dose aspirin, and 36 % used regular- or high-dose aspirin. Compared with nonuse of aspirin, the HRs (95 % CI) for incidence of aspirin-sensitive cancers were 0.87 (0.72-1.06) for regular to high doses of aspirin use, 0.95 (0.80-1.13) for aspirin use 6+ times per week, and 0.93 (0.74-1.17) for aspirin use for 10+ years. For cumulative aspirin use, HR (95 % CI) was 0.87 (0.70-1.09) for >60,000 mg of aspirin per year and 0.95 (0.75-1.21) for >280,000 mg of aspirin in their lifetime, versus nonuse of aspirin. Results were similar for the all-cause cancer death as an endpoint, with a significant inverse association observed between lifetime aspirin dose and cancer mortality [<95,000 mg vs nonuser HR 0.76 (0.61-0.95)]. CONCLUSIONS: These findings suggest that aspirin use may prevent incident breast, colon, pancreatic, and ovarian cancer in elderly women.

3 Article Diabetes, antidiabetic medications, and pancreatic cancer risk: an analysis from the International Pancreatic Cancer Case-Control Consortium. 2014

Bosetti, C / Rosato, V / Li, D / Silverman, D / Petersen, G M / Bracci, P M / Neale, R E / Muscat, J / Anderson, K / Gallinger, S / Olson, S H / Miller, A B / Bas Bueno-de-Mesquita, H / Scelo, G / Janout, V / Holcatova, I / Lagiou, P / Serraino, D / Lucenteforte, E / Fabianova, E / Ghadirian, P / Baghurst, P A / Zatonski, W / Foretova, L / Fontham, E / Bamlet, W R / Holly, E A / Negri, E / Hassan, M / Prizment, A / Cotterchio, M / Cleary, S / Kurtz, R C / Maisonneuve, P / Trichopoulos, D / Polesel, J / Duell, E J / Boffetta, P / La Vecchia, C. ·Department of Epidemiology, IRCCS - Istituto di Ricerche Farmacologiche 'Mario Negri', Milan, Italy cristina.bosetti@marionegri.it. · Department of Epidemiology, IRCCS - Istituto di Ricerche Farmacologiche 'Mario Negri', Milan, Italy. · M.D. Anderson Cancer Center, University of Texas, Houston. · Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda. · Department of Health Sciences Research, Medicine and Medical Genetics, Mayo Clinic, Rochester. · Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, USA. · Queensland Institute of Medical Research, Brisbane, Australia. · Department of Public Health Sciences, Penn State University, Penn State. · Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, USA. · University Health Network, Department of Surgery, University of Toronto, Toronto, Canada. · Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, USA. · Dalla Lana School of Public Health, University of Toronto, Toronto, Canada. · National Institute for Public Health and the Environment (RIVM), Bilthoven Department of Gastroenterology and Hepatology, University Medical Center Utrecht (UMCU), Utrecht, The Netherlands Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK. · International Agency for Research on Cancer (IARC), Lyon, France. · Department of Preventive Medicine, Faculty of Medicine, Palacky University, Olomouc. · Institute of Hygiene and Epidemiology, 1st Faculty of Medicine, Charles University in Prague, Prague, Czech Republic. · Department of Epidemiology, Harvard School of Public Health, Boston, USA Department of Hygiene, Epidemiology and Medical Statistics, School of Medicine, University of Athens, Athens, Greece. · Unit of Epidemiology and Biostatistics, CRO Aviano National Cancer Institute, IRCCS, Aviano. · Department of Preclinical and Clinical Pharmacology Mario Aiazzi Mancini, Università degli Studi di Firenze, Florence, Italy. · Regional Authority of Public Health in Banská Bystrica, Banská Bystrica, Slovakia. · Department of Epidemiology, IRCCS - Istituto di Ricerche Farmacologiche 'Mario Negri', Milan, Italy M.D. Anderson Cancer Center, University of Texas, Houston Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda Department of Health Sciences Research, Medicine and Medical Genetics, Mayo Clinic, Rochester Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, USA Queensland Institute of Medical Research, Brisbane, Australia Department of Public Health Sciences, Penn State University, Penn State Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, USA University Health Network, Department of Surgery, University of Toronto, Toronto, Canada Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, USA Dalla Lana School of Public Health, University of Toronto, Toronto, Canada National Institute for Public Health and the Environment (RIVM), Bilthoven Department of Gastroenterology and Hepatology, University Medical Center Utrecht (UMCU), Utrecht, The Netherlands Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK International Agency for Research on Cancer (IARC), Lyon, France Department of Preventive Medicine, Faculty of Medicine, Palacky University, Olomouc Institute of Hygiene and Epidemiology, 1st Faculty of Medicine, Charles University in Prague, Prague, Czech Republic Department of Epidemiology, Harvard School of Public Health, Boston, USA Department of Hygiene, Epidemiology and Medical Statistics, School of Medicine, University of Athens, Athens, Greece Unit of Epidemiology and Biostatistics, CRO Aviano National Cancer Institute, IRCCS, Aviano Department of Preclinical and Clinical Pharmacology Mario Aiazzi Mancini, Università degli Studi di Firenze, Florence, Italy Regional Authority of Public Health in Banská Bystrica, Banská Bystrica, Slovakia Public Health, Women · Public Health, Women's and Children's Hospital, Adelaide, SA, Australia. · Cancer Center and Institute of Oncology, Warsaw, Poland. · Department of Cancer Epidemiology and Genetics, Masaryk Memorial Cancer Institute, Institute and MF MU, Brno, Czech Republic. · Louisiana State University School of Public Health, New Orleans, USA. · Dalla Lana School of Public Health, University of Toronto, Toronto, Canada Cancer Care Ontario, Toronto, Canada. · Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, USA. · Division of Epidemiology and Biostatistics, European Institute of Oncology, Milan, Italy. · Department of Epidemiology, Harvard School of Public Health, Boston, USA. · Unit of Nutrition, Environment and Cancer, Catalan Institute of Oncology (ICO-IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain. · The Tisch Cancer Institute and Institute for Translational Epidemiology, Icahn School of Medicine at Mount Sinai, New York, USA. · Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy. ·Ann Oncol · Pubmed #25057164.

ABSTRACT: BACKGROUND: Type 2 diabetes mellitus has been associated with an excess risk of pancreatic cancer, but the magnitude of the risk and the time-risk relationship are unclear, and there is limited information on the role of antidiabetic medications. PATIENTS AND METHODS: We analyzed individual-level data from 15 case-control studies within the Pancreatic Cancer Case-Control Consortium, including 8305 cases and 13 987 controls. Pooled odds ratios (ORs) were estimated from multiple logistic regression models, adjusted for relevant covariates. RESULTS: Overall, 1155 (15%) cases and 1087 (8%) controls reported a diagnosis of diabetes 2 or more years before cancer diagnosis (or interview, for controls), corresponding to an OR of 1.90 (95% confidence interval, CI, 1.72-2.09). Consistent risk estimates were observed across strata of selected covariates, including body mass index and tobacco smoking. Pancreatic cancer risk decreased with duration of diabetes, but a significant excess risk was still evident 20 or more years after diabetes diagnosis (OR 1.30, 95% CI 1.03-1.63). Among diabetics, long duration of oral antidiabetic use was associated with a decreased pancreatic cancer risk (OR 0.31, 95% CI 0.14-0.69, for ≥15 years). Conversely, insulin use was associated with a pancreatic cancer risk in the short term (OR 5.60, 95% CI 3.75-8.35, for <5 years), but not for longer duration of use (OR 0.95, 95% CI 0.53-1.70, for ≥15 years). CONCLUSION: This study provides the most definitive quantification to date of an excess risk of pancreatic cancer among diabetics. It also shows that a 30% excess risk persists for more than two decades after diabetes diagnosis, thus supporting a causal role of diabetes in pancreatic cancer. Oral antidiabetics may decrease the risk of pancreatic cancer, whereas insulin showed an inconsistent duration-risk relationship.

4 Article Cholecystectomy, gallstones, tonsillectomy, and pancreatic cancer risk: a population-based case-control study in Minnesota. 2014

Zhang, J / Prizment, A E / Dhakal, I B / Anderson, K E. ·1] Department of Epidemiology, Indiana University, Richard M. Fairbanks School of Public Health at IUPUI, Indianapolis, IN 46202, USA [2] Melvin and Bren Simon Cancer Center, Indiana University, Indianapolis, IN 46202, USA. · Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN 55455, USA. · Department of Biostatistics, Fay W. Boozman College of Public Health, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. · 1] Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN 55455, USA [2] Masonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA. ·Br J Cancer · Pubmed #24667646.

ABSTRACT: BACKGROUND: Associations between medical conditions and pancreatic cancer risk are controversial and are thus evaluated in a study conducted during 1994-1998 in Minnesota. METHODS: Cases (n=215) were ascertained from hospitals in the metropolitan area of the Twin Cities and the Mayo Clinic. Controls (n=676) were randomly selected from the general population and frequency matched to cases by age and sex. The history of medical conditions was gathered with a questionnaire during in-person interviews. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using unconditional logistic regression. RESULTS: After adjustment for confounders, subjects who had cholecystectomy or gallstones experienced a significantly higher risk of pancreatic cancer than those who did not (OR (95% CI): 2.11 (1.32-3.35) for cholecystectomy and 1.97 (1.23-3.12) for gallstones), whereas opposite results were observed for tonsillectomy (0.67 (0.48-0.94)). Increased risk associated with cholecystectomy was the greatest when it occurred ≤ 2 years before the cancer diagnosis (5.93 (2.36-15.7)) but remained statistically significant when that interval was ≥ 20 years (2.27 (1.16-4.32)). CONCLUSIONS: Cholecystectomy, gallstones, and tonsillectomy were associated with an altered risk of pancreatic cancer. Our study suggests that cholecystectomy increased risk but reverse causality may partially account for high risk associated with recent cholecystectomy.

5 Article Genetic variability in energy balance and pancreatic cancer risk in a population-based case-control study in Minnesota. 2014

Zhang, Jianjun / Dhakal, Ishwori B / Zhang, Xuemei / Prizment, Anna E / Anderson, Kristin E. ·From the *Department of Epidemiology, Indiana University Richard M. Fairbanks School of Public Health at IUPUI; †Melvin Bren Simon Cancer Center, Indiana University, Indianapolis, IN; ‡Department of Biostatistics, Fay W. Boozman College of Public Health, University of Arkansas for Medical Sciences, Little Rock, AR; §Department of Molecular Biology, College of Life Sciences, Hebei United University, Tangshan, China; ∥Division of Epidemiology and Community Health, School of Public Health, and ¶Masonic Cancer Center, University of Minnesota, Minneapolis, MN. ·Pancreas · Pubmed #24201779.

ABSTRACT: OBJECTIVES: Accumulating evidence suggests that energy imbalance plays a role in pancreatic carcinogenesis. However, it remains unclear whether single-nucleotide polymorphisms (SNPs) in genes regulating energy homeostasis influence pancreatic cancer risk. We investigated this question in a case-control study conducted from 1994 to 1998. METHODS: Patients (n = 173) were ascertained from hospitals in the Twin Cities and Mayo Clinic, Minnesota. Control subjects (n = 476) were identified from the general population and frequency matched to patients by age and sex. Seven SNPs were evaluated in relation to pancreatic cancer using unconditional logistic regression. RESULTS: After adjustment for confounders, the leucine/proline or proline/proline genotype of the neuropeptide Y (NPY) gene rs16139 was associated with a lower risk than the leucine/leucine genotype (odds ratio, 0.40 [95% confidence interval, 0.15-0.91]). Conversely, an increased risk was observed for the glycine/arginine or arginine/arginine genotype of the adrenoceptor β2, surface (ADRB2) gene rs1042713 as compared with the glycine/glycine genotype (odds ratio, 1.52 [95% confidence interval, 1.01-2.31]). CONCLUSIONS: This study first reveals that SNPs in genes modulating energy intake (NPY) and energy expenditure (ADRB2) altered pancreatic cancer risk. If confirmed by other studies, our findings may shed new light on the etiology and prevention of pancreatic cancer.

6 Article Duration of diabetes and pancreatic cancer in a case-control study in the Midwest and the Iowa Women's Health Study (IWHS) cohort. 2013

Henry, Sarah A / Prizment, Anna E / Anderson, Kristin E. ·Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, University of Minnesota Masonic Cancer Center, Minneapolis, MN 55455, USA. ·JOP · Pubmed #23669472.

ABSTRACT: CONTEXT: Studies have shown a relationship between history of diabetes and the risk of pancreatic cancer; however, the temporal relation between diabetes and pancreatic cancer is not clearly established. OBJECTIVES: Diabetes and diabetes duration were examined in relation to pancreatic cancer in a population-based case-control study and prospective cohort. METHODS: Case-control study: pancreatic cancer cases (n=200) from the Midwest were frequency matched by age and sex to population controls (n=673). Logistic regression yielded odds ratios (ORs) and 95% confidence intervals (95% CI). Iowa Women's Health Study (IWHS) cohort: 292 incident pancreatic cancer cases occurred between 1986-2008 among 36,084 post-menopausal, initially cancer-free women. Diabetes status and diagnosis age were ascertained at baseline and follow-ups. Proportional hazards regression yielded hazard ratios (HR, 95% CI) for pancreatic cancer in relation to baseline diabetes. Time-dependent analyses accounted for diabetes diagnosed after baseline. A nested-case control analysis assessed diabetes duration as a risk factor. RESULTS: In the case-control study, compared to participants without diabetes, the multivariate ORs (95% CI) for pancreatic cancer were 2.35 (1.24-4.47) for those with diabetes and 4.00 (0.94-16.9), 2.79 (0.97-8.04), and 2.40 (0.97-5.98) for diabetes durations of 2-5 years, 5.1-10 years, and more than 10 years, respectively. In IWHS, compared to no diabetes, multivariate-adjusted HRs for pancreatic cancer were 1.86 (1.23-2.83) for baseline diabetes and 1.94 (1.40-2.69) adding diabetes during follow-up. In an IWHS nested case-control analysis, ORs were 1.70 (0.78-3.67), 2.62 (1.48-4.65), and 2.10 (1.36-3.24) for diabetes durations of 2-5 years, 5.1-10 years and more than 10 years, respectively, versus no diabetes. CONCLUSIONS: Diabetes is associated with pancreatic cancer risk and this is similar across different duration categories.

7 Article Genes related to diabetes may be associated with pancreatic cancer in a population-based case-control study in Minnesota. 2012

Prizment, Anna E / Gross, Myron / Rasmussen-Torvik, Laura / Peacock, James M / Anderson, Kristin E. ·Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN 55455, USA. prizm001@umn.edu ·Pancreas · Pubmed #22015968.

ABSTRACT: OBJECTIVES: Type 2 diabetes is associated with increased pancreatic cancer risk; however, the nature of this relationship is not clear. We examined the link between 10 diabetes-related single-nucleotide polymorphisms and pancreatic cancer in a case-control study conducted in 1994 to 1998. METHODS: Cases (n = 162) were ascertained from hospitals in the Twin Cities and Mayo Clinic, Minn. Controls (n = 540) from the general population were frequency matched by age, sex, and race. Unconditional logistic regression provided odds ratios of pancreatic cancer and 95% confidence intervals (95% CIs). RESULTS: In a multivariate-adjusted model, a significant association was observed only for rs780094 in the glucokinase regulator (GCKR) gene: odds ratios for pancreatic cancer were 1.00 for TT, 1.35 (95% CI, 0.71-2.58) for CT, and 2.14 (95% CI, 1.12-4.08) for CC genotypes (P trend = 0.01) and did not change after the adjustment for diabetes. CONCLUSIONS: This study provides the first evidence that GCKR rs780094, a single-nucleotide polymorphism related to diabetes, may be associated with pancreatic cancer risk. Although the results from this analysis are preliminary, there is a biologic plausibility for such an association.