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Pancreatic Neoplasms: HELP
Articles by Simin Liu
Based on 3 articles published since 2010
(Why 3 articles?)

Between 2010 and 2020, Simin Liu 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 Elevation of circulating branched-chain amino acids is an early event in human pancreatic adenocarcinoma development. 2014

Mayers, Jared R / Wu, Chen / Clish, Clary B / Kraft, Peter / Torrence, Margaret E / Fiske, Brian P / Yuan, Chen / Bao, Ying / Townsend, Mary K / Tworoger, Shelley S / Davidson, Shawn M / Papagiannakopoulos, Thales / Yang, Annan / Dayton, Talya L / Ogino, Shuji / Stampfer, Meir J / Giovannucci, Edward L / Qian, Zhi Rong / Rubinson, Douglas A / Ma, Jing / Sesso, Howard D / Gaziano, John Michael / Cochrane, Barbara B / Liu, Simin / Wactawski-Wende, Jean / Manson, JoAnn E / Pollak, Michael N / Kimmelman, Alec C / Souza, Amanda / Pierce, Kerry / Wang, Thomas J / Gerszten, Robert E / Fuchs, Charles S / Vander Heiden, Matthew G / Wolpin, Brian M. ·Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA. · Department of Etiology and Carcinogenesis, Cancer Institute and Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China. · Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA. · Department of Epidemiology, Harvard School of Public Health, Boston, MA. · Broad Institute of MIT and Harvard University, Cambridge, MA. · Department of Biostatistics, Harvard School of Public Health, Boston, MA. · Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA. · Division of Genomic Stability and DNA repair, Department of Radiation Oncology, Dana- Farber Cancer Institute, Boston, MA 02215. · Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA. · Department of Nutrition, Harvard School of Public Health, Boston, MA. · Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA. · Massachusetts Veterans Epidemiology Research and Information Center (MAVERIC), VA Boston Healthcare System. · University of Washington School of Nursing, Seattle, WA. · Departments of Epidemiology and Medicine, Brown University, Providence, RI. · Department of Social and Preventive Medicine, University at Buffalo, SUNY, Buffalo, NY. · Departments of Oncology and Medicine, McGill University, Montreal, QC, Canada. · Division of Cardiovascular Medicine, Vanderbilt University, Nashville, TN. · Cardiology Division, Massachusetts General Hospital, and Harvard Medical School, Boston, MA. · Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA. ·Nat Med · Pubmed #25261994.

ABSTRACT: Most patients with pancreatic ductal adenocarcinoma (PDAC) are diagnosed with advanced disease and survive less than 12 months. PDAC has been linked with obesity and glucose intolerance, but whether changes in circulating metabolites are associated with early cancer progression is unknown. To better understand metabolic derangements associated with early disease, we profiled metabolites in prediagnostic plasma from individuals with pancreatic cancer (cases) and matched controls from four prospective cohort studies. We find that elevated plasma levels of branched-chain amino acids (BCAAs) are associated with a greater than twofold increased risk of future pancreatic cancer diagnosis. This elevated risk was independent of known predisposing factors, with the strongest association observed among subjects with samples collected 2 to 5 years before diagnosis, when occult disease is probably present. We show that plasma BCAAs are also elevated in mice with early-stage pancreatic cancers driven by mutant Kras expression but not in mice with Kras-driven tumors in other tissues, and that breakdown of tissue protein accounts for the increase in plasma BCAAs that accompanies early-stage disease. Together, these findings suggest that increased whole-body protein breakdown is an early event in development of PDAC.

3 Article An absolute risk model to identify individuals at elevated risk for pancreatic cancer in the general population. 2013

Klein, Alison P / Lindström, Sara / Mendelsohn, Julie B / Steplowski, Emily / Arslan, Alan A / Bueno-de-Mesquita, H Bas / Fuchs, Charles S / Gallinger, Steven / Gross, Myron / Helzlsouer, Kathy / Holly, Elizabeth A / Jacobs, Eric J / Lacroix, Andrea / Li, Donghui / Mandelson, Margaret T / Olson, Sara H / Petersen, Gloria M / Risch, Harvey A / Stolzenberg-Solomon, Rachael Z / Zheng, Wei / Amundadottir, Laufey / Albanes, Demetrius / Allen, Naomi E / Bamlet, William R / Boutron-Ruault, Marie-Christine / Buring, Julie E / Bracci, Paige M / Canzian, Federico / Clipp, Sandra / Cotterchio, Michelle / Duell, Eric J / Elena, Joanne / Gaziano, J Michael / Giovannucci, Edward L / Goggins, Michael / Hallmans, Göran / Hassan, Manal / Hutchinson, Amy / Hunter, David J / Kooperberg, Charles / Kurtz, Robert C / Liu, Simin / Overvad, Kim / Palli, Domenico / Patel, Alpa V / Rabe, Kari G / Shu, Xiao-Ou / Slimani, Nadia / Tobias, Geoffrey S / Trichopoulos, Dimitrios / Van Den Eeden, Stephen K / Vineis, Paolo / Virtamo, Jarmo / Wactawski-Wende, Jean / Wolpin, Brian M / Yu, Herbert / Yu, Kai / Zeleniuch-Jacquotte, Anne / Chanock, Stephen J / Hoover, Robert N / Hartge, Patricia / Kraft, Peter. ·Department of Oncology, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland, United States of America ; Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins School of Medicine, Baltimore, Maryland, United States of America ; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America. ·PLoS One · Pubmed #24058443.

ABSTRACT: PURPOSE: We developed an absolute risk model to identify individuals in the general population at elevated risk of pancreatic cancer. PATIENTS AND METHODS: Using data on 3,349 cases and 3,654 controls from the PanScan Consortium, we developed a relative risk model for men and women of European ancestry based on non-genetic and genetic risk factors for pancreatic cancer. We estimated absolute risks based on these relative risks and population incidence rates. RESULTS: Our risk model included current smoking (multivariable adjusted odds ratio (OR) and 95% confidence interval: 2.20 [1.84-2.62]), heavy alcohol use (>3 drinks/day) (OR: 1.45 [1.19-1.76]), obesity (body mass index >30 kg/m(2)) (OR: 1.26 [1.09-1.45]), diabetes >3 years (nested case-control OR: 1.57 [1.13-2.18], case-control OR: 1.80 [1.40-2.32]), family history of pancreatic cancer (OR: 1.60 [1.20-2.12]), non-O ABO genotype (AO vs. OO genotype) (OR: 1.23 [1.10-1.37]) to (BB vs. OO genotype) (OR 1.58 [0.97-2.59]), rs3790844(chr1q32.1) (OR: 1.29 [1.19-1.40]), rs401681(5p15.33) (OR: 1.18 [1.10-1.26]) and rs9543325(13q22.1) (OR: 1.27 [1.18-1.36]). The areas under the ROC curve for risk models including only non-genetic factors, only genetic factors, and both non-genetic and genetic factors were 58%, 57% and 61%, respectively. We estimate that fewer than 3/1,000 U.S. non-Hispanic whites have more than a 5% predicted lifetime absolute risk. CONCLUSION: Although absolute risk modeling using established risk factors may help to identify a group of individuals at higher than average risk of pancreatic cancer, the immediate clinical utility of our model is limited. However, a risk model can increase awareness of the various risk factors for pancreatic cancer, including modifiable behaviors.