Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Pancreatic Neoplasms: HELP
Articles by Michael S. Simon
Based on 3 articles published since 2010
(Why 3 articles?)
||||

Between 2010 and 2020, M. S. Simon wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Prospective analysis of association between statins and pancreatic cancer risk in the Women's Health Initiative. 2016

Simon, Michael S / Desai, Pinkal / Wallace, Robert / Wu, Chunyuan / Howard, Barbara V / Martin, Lisa W / Schlecht, Nicolas / Liu, Simin / Jay, Allison / LeBlanc, Erin S / Rohan, Thomas / Manson, JoAnn. ·Department of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA. simonm@karmanos.org. · Barbara Ann Karmanos Cancer Institute, 4100 John R, 4221 HWCRC, Detroit, MI, USA. simonm@karmanos.org. · Weill Cornell Medical College, New York, NY, USA. · Department of Epidemiology, University of Iowa College of Public Health, Iowa City, IA, USA. · Fred Hutchinson Cancer Research Center, Seattle, WA, USA. · MedStar Health Research Institute and Georgetown/Howard Universities Center for Clinical and Translational Sciences, Washington, DC, USA. · George Washington University, Washington, DC, USA. · Albert Einstein College of Medicine, Bronx, NY, USA. · UCLA School of Public Health, Los Angeles, CA, USA. · St John's Hospital and Medical Center, Detroit, MI, USA. · Center for Health Research, Kaiser Permanente NW, Portland, OR, USA. · Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. ·Cancer Causes Control · Pubmed #26857832.

ABSTRACT: PURPOSE: To determine whether HMG-CoA reductase inhibitors (statins) are associated with a lower risk of pancreatic cancer. METHODS: The population included 160,578 postmenopausal women enrolled in the Women's Health Initiative (WHI) in which 385 incident cases of pancreatic cancer were identified over an average of 8.69 (SD ±4.59) years. All diagnoses were confirmed by medical record and pathology review. Information on statin use and other risk factors was collected at baseline and during follow-up. Multivariable-adjusted hazards ratios (HRs) and 95 % confidence intervals (CIs) evaluating the relationship between prior statin use (at baseline only as well as in a time-dependent manner) and risk of pancreatic cancer were computed from Cox proportional hazards regression analyses after adjusting for appropriate confounders. We also evaluated the effect of statin type, potency, lipophilic status, and duration of use. All statistical tests were two-sided. RESULTS: Statins were used at baseline by 12,243 (7.5 %) women. The annualized rate of pancreatic cancer in statin users and nonusers, respectively, was 0.0298 versus 0.0271 %. The multivariable-adjusted HR for statin users versus nonusers at baseline was 0.92 and 95 % CI 0.57-1.48. In a time-dependent model, the HR for low-potency statins was 0.46, 95 % CI 0.20-1.04. There was no significant effect seen by statin lipophilicity or duration of use. CONCLUSIONS: There was no significant relationship between statins and pancreatic cancer risk in the WHI; however, there was a marginal inverse association noted for low-potency statins. Analyses of larger numbers of cases are needed to further explore this relationship.

2 Article Diabetes and risk of pancreatic cancer: a pooled analysis from the pancreatic cancer cohort consortium. 2013

Elena, Joanne W / Steplowski, Emily / Yu, Kai / Hartge, Patricia / Tobias, Geoffrey S / Brotzman, Michelle J / Chanock, Stephen J / Stolzenberg-Solomon, Rachael Z / Arslan, Alan A / Bueno-de-Mesquita, H Bas / Helzlsouer, Kathy / Jacobs, Eric J / LaCroix, Andrea / Petersen, Gloria / Zheng, Wei / Albanes, Demetrius / Allen, Naomi E / Amundadottir, Laufey / Bao, Ying / Boeing, Heiner / Boutron-Ruault, Marie-Christine / Buring, Julie E / Gaziano, J Michael / Giovannucci, Edward L / Duell, Eric J / Hallmans, Göran / Howard, Barbara V / Hunter, David J / Hutchinson, Amy / Jacobs, Kevin B / Kooperberg, Charles / Kraft, Peter / Mendelsohn, Julie B / Michaud, Dominique S / Palli, Domenico / Phillips, Lawrence S / Overvad, Kim / Patel, Alpa V / Sansbury, Leah / Shu, Xiao-Ou / Simon, Michael S / Slimani, Nadia / Trichopoulos, Dimitrios / Visvanathan, Kala / Virtamo, Jarmo / Wolpin, Brian M / Zeleniuch-Jacquotte, Anne / Fuchs, Charles S / Hoover, Robert N / Gross, Myron. ·Division of Cancer Control and Population Science, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA. elenajw@mail.nih.gov ·Cancer Causes Control · Pubmed #23112111.

ABSTRACT: PURPOSE: Diabetes is a suspected risk factor for pancreatic cancer, but questions remain about whether it is a risk factor or a result of the disease. This study prospectively examined the association between diabetes and the risk of pancreatic adenocarcinoma in pooled data from the NCI pancreatic cancer cohort consortium (PanScan). METHODS: The pooled data included 1,621 pancreatic adenocarcinoma cases and 1,719 matched controls from twelve cohorts using a nested case-control study design. Subjects who were diagnosed with diabetes near the time (<2 years) of pancreatic cancer diagnosis were excluded from all analyses. All analyses were adjusted for age, race, gender, study, alcohol use, smoking, BMI, and family history of pancreatic cancer. RESULTS: Self-reported diabetes was associated with a forty percent increased risk of pancreatic cancer (OR = 1.40, 95 % CI: 1.07, 1.84). The association differed by duration of diabetes; risk was highest for those with a duration of 2-8 years (OR = 1.79, 95 % CI: 1.25, 2.55); there was no association for those with 9+ years of diabetes (OR = 1.02, 95 % CI: 0.68, 1.52). CONCLUSIONS: These findings provide support for a relationship between diabetes and pancreatic cancer risk. The absence of association in those with the longest duration of diabetes may reflect hypoinsulinemia and warrants further investigation.

3 Article Glycemic index, glycemic load, and the risk of pancreatic cancer among postmenopausal women in the women's health initiative observational study and clinical trial. 2010

Simon, M S / Shikany, J M / Neuhouser, M L / Rohan, T / Nirmal, K / Cui, Y / Abrams, J / Anonymous1210668. ·Karmanos Cancer Institute, Department of Oncology, Wayne State University, 4100 John R, 4221, HWCRC, Detroit, MI, USA. Simonm@karmanos.org ·Cancer Causes Control · Pubmed #20711806.

ABSTRACT: BACKGROUND: Several reports have suggested that conditions associated with hyperinsulinemia and insulin resistance, such as diets high in carbohydrates, may influence the risk of pancreatic cancer, although results from prior studies have been mixed. METHODS: We utilized data from the population-based women's health initiative (WHI) cohort to determine whether dietary factors that are associated with increased postprandial blood glucose levels are also associated with an increased risk of pancreatic cancer. The WHI included 161,809 postmenopausal women of ages 50-79, in which 332 cases of pancreatic cancer were identified over a median of 8 years of follow-up; 287 of these cases met the criteria for analysis. A validated 122-item food frequency questionnaire was used to estimate dietary glycemic load (GL), glycemic index (GI), total and available carbohydrates, fructose and sucrose. Baseline questionnaires and physical exams provided information on demographic, medical, lifestyle, and anthropometric characteristics. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between the exposures of interest and pancreatic cancer risk, with adjustment for potential confounders. RESULTS: Dietary GL, GI, carbohydrates, fructose, and sucrose were not associated with increased risk of pancreatic cancer. The multivariable adjusted HR for the highest vs. the lowest quartile of GL was 0.80 (95% CI = 0.55-1.15, trend p = 0.31) and 1.13 (95% CI = 0.78-1.63, trend p = 0.94) for GI. The results remained negative when individuals with a history of diabetes were excluded. CONCLUSIONS: Our results do not support the hypothesis that dietary intake of carbohydrates is associated with increased risk of pancreatic cancer.