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Pancreatic Neoplasms: HELP
Articles by Lin Jiao
Based on 13 articles published since 2010
(Why 13 articles?)
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Between 2010 and 2020, Li Jiao wrote the following 13 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Clinical Trial Dietary consumption of advanced glycation end products and pancreatic cancer in the prospective NIH-AARP Diet and Health Study. 2015

Jiao, Li / Stolzenberg-Solomon, Rachael / Zimmerman, Thea Palmer / Duan, Zhigang / Chen, Liang / Kahle, Lisa / Risch, Adam / Subar, Amy F / Cross, Amanda J / Hollenbeck, Albert / Vlassara, Helen / Striker, Gary / Sinha, Rashmi. ·From the Sections of Gastroenterology and Hepatology (LJ and LC) and Health Services Research (LJ, ZD, and LC), Department of Medicine, Baylor College of Medicine, Houston, TX · the Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics (RS-S and RS) and the Applied Research Program, Division of Cancer Control and Population Sciences (AFS), National Cancer Institute, NIH, Rockville, MD · Westat, Rockville, MD (TPZ) · Information Management Services, Rockville, MD (LK and AR) · the Department of Epidemiology and Biostatistics, School of Public Health, Faculty of Medicine, Imperial College London, London, United Kingdom (AJC) · the Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, NY (HV and GS) · and AARP, Washington, DC (AH). ·Am J Clin Nutr · Pubmed #25527756.

ABSTRACT: BACKGROUND: Advanced glycation end products (AGEs) are a heterogeneous group of compounds present in uncooked foods as well as in foods cooked at high temperatures. AGEs have been associated with insulin resistance, oxidative stress, and chronic inflammation in patients with diabetes. Dietary AGEs are an important contributor to the AGE pool in the body. N(ϵ)-(carboxymethyl)lysine (CML) AGE is one of the major biologically and chemically well-characterized AGE markers. The consumption of red meat, which is CML-AGE rich, has been positively associated with pancreatic cancer in men. OBJECTIVES: With the use of a published food CML-AGE database, we estimated the consumption of CML AGE in the prospective NIH-AARP Diet and Health Study and evaluated the association between CML-AGE consumption and pancreatic cancer and the mediating effect of CML AGE on the association between red meat consumption and pancreatic cancer. DESIGN: Multivariate Cox proportional hazard regression models were used to estimate HRs and 95% CIs for pancreatic cancer. RESULTS: During an average of 10.5 y of follow-up, we identified 2193 pancreatic cancer cases (1407 men and 786 women) from 528,251 subjects. With the comparison of subjects in the fifth and the first quintiles of CML-AGE consumption, we observed increased pancreatic cancer risk in men (HR: 1.43; 95% CI: 1.06, 1.93, P-trend = 0.003) but not women (HR: 1.14; 95% CI: 0.76, 1.72, P-trend = 0.42). Men in the highest quintile of red meat consumption had higher risk of pancreatic cancer (HR: 1.35; 95% CI: 1.07, 1.70), which attenuated after adjustment for CML-AGE consumption (HR: 1.20; 95% CI: 0.95, 1.53). CONCLUSION: Dietary CML-AGE consumption was associated with modestly increased risk of pancreatic cancer in men and may partially explain the positive association between red meat and pancreatic cancer.

2 Article lncRNA SLC7A11-AS1 Promotes Chemoresistance by Blocking SCF 2020

Yang, Qingzhu / Li, Kai / Huang, Xuemei / Zhao, Chen / Mei, Yu / Li, Xinyuan / Jiao, Lin / Yang, Huanjie. ·School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China. · School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China. Electronic address: yanghj@hit.edu.cn. ·Mol Ther Nucleic Acids · Pubmed #32036249.

ABSTRACT: Drug resistance is the major obstacle of gemcitabine-based chemotherapy for the treatment of pancreatic ductal adenocarcinoma (PDAC). Many long non-coding RNAs (lncRNAs) are reported to play vital roles in cancer initiation and progression. Here, we report that lncRNA SLC7A11-AS1 is involved in gemcitabine resistance of PDAC. SLC7A11-AS1 is overexpressed in PDAC tissues and gemcitabine-resistant cell lines. Knockdown of SLC7A11-AS1 weakens the PDAC stemness and potentiates the sensitivity of resistant PDAC cells toward gemcitabine in vitro and in vivo. SLC7A11-AS1 promotes chemoresistance through reducing intracellular reactive oxygen species (ROS) by stabilizing nuclear factor erythroid-2-related factor 2 (NRF2), the key regulator in antioxidant defense. Mechanically, SLC7A11-AS1 is co-localized with β-TRCP1 in the nucleus. The exon 3 of SLC7A11-AS1 interacts with the F-box motif of β-TRCP1, the critical domain that recruits β-TRCP1 to the SCF

3 Article Anti-Hypertensive Medication Use, Soluble Receptor for Glycation End Products and Risk of Pancreatic Cancer in the Women's Health Initiative Study. 2018

Wang, Zhensheng / White, Donna L / Hoogeveen, Ron / Chen, Liang / Whitsel, Eric A / Richardson, Peter A / Virani, Salim S / Garcia, Jose M / El-Serag, Hashem B / Jiao, Li. ·Section of Epidemiology and Population Sciences, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. zhenshew@bcm.edu. · Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. dwhite1@bcm.edu. · Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael E. DeBakey VA Medical Center, Houston, TX 77030, USA. dwhite1@bcm.edu. · Section of Health Services Research, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. dwhite1@bcm.edu. · Texas Medical Center Digestive Disease Center, Houston, TX 77030, USA. dwhite1@bcm.edu. · Dan L. Duncan Cancer Center at Baylor College of Medicine, Houston, TX 77030, USA. dwhite1@bcm.edu. · Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey VA Medical Center, Houston, TX 77030, USA. dwhite1@bcm.edu. · Section of Atherosclerosis and Vascular Medicine, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. ronh@bcm.edu. · Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. liangc@bcm.edu. · Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael E. DeBakey VA Medical Center, Houston, TX 77030, USA. liangc@bcm.edu. · Section of Health Services Research, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. liangc@bcm.edu. · Departments of Epidemiology and Medicine, Gillings School of Global Public Health and School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. eric_whitsel@med.unc.edu. · Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael E. DeBakey VA Medical Center, Houston, TX 77030, USA. peter.richardson2@va.gov. · Section of Health Services Research, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. peter.richardson2@va.gov. · Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael E. DeBakey VA Medical Center, Houston, TX 77030, USA. virani@bcm.edu. · Section of Health Services Research, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. virani@bcm.edu. · Section of Atherosclerosis and Vascular Medicine, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. virani@bcm.edu. · Geriatric Research Education and Clinical Center (GRECC), Puget Sound Department of Veterans Affairs Medical Center, Seattle, WA 98108, USA. Jg77@uw.edu. · Section of Endocrinology, Department of Medicine, University of Washington, Seattle, WA 98195, USA. Jg77@uw.edu. · Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. hasheme@bcm.edu. · Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael E. DeBakey VA Medical Center, Houston, TX 77030, USA. hasheme@bcm.edu. · Section of Health Services Research, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. hasheme@bcm.edu. · Texas Medical Center Digestive Disease Center, Houston, TX 77030, USA. hasheme@bcm.edu. · Dan L. Duncan Cancer Center at Baylor College of Medicine, Houston, TX 77030, USA. hasheme@bcm.edu. · Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. jiao@bcm.edu. · Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael E. DeBakey VA Medical Center, Houston, TX 77030, USA. jiao@bcm.edu. · Section of Health Services Research, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. jiao@bcm.edu. · Texas Medical Center Digestive Disease Center, Houston, TX 77030, USA. jiao@bcm.edu. · Dan L. Duncan Cancer Center at Baylor College of Medicine, Houston, TX 77030, USA. jiao@bcm.edu. · Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey VA Medical Center, Houston, TX 77030, USA. jiao@bcm.edu. ·J Clin Med · Pubmed #30072610.

ABSTRACT: Pancreatic cancer is the fourth leading cause of cancer death. Soluble receptor for glycation end products (sRAGE), which is modulated by anti-hypertensive (HT) medications, has been inversely associated with pancreatic cancer. However, the association between commonly used anti-HT medications and risk of pancreatic cancer is unknown. A total of 145,551 postmenopausal women from the Women Health Initiative (WHI) Study were included in analysis. Use of angiotensin converting enzyme inhibitors (ACEi), β-blockers, calcium channel blockers (CCBs) and diuretics was ascertained at baseline (1993⁻1998). Baseline sRAGE levels were measured among a subset of 2104 participants using an immunoassay. Multivariable Cox proportional hazard regression model was performed to estimate hazard ratios (HRs) and its 95% confidence intervals (CIs) for pancreatic cancer in association with anti-HT medications. Increased risk of pancreatic cancer was found among users of short-acting CCB (HR = 1.66, 95% CI: 1.20⁻2.28) and long-term (≥3 years) users of short-acting CCB (HR = 2.07, 95% CI: 1.42⁻3.02) compared to users of other anti-HT medications. Average sRAGE levels were lower in short-acting CCB users than users of other anti-HT medications (1173 versus 1454 pg/mL,

4 Article A prospective study of soluble receptor for advanced glycation end products and adipokines in association with pancreatic cancer in postmenopausal women. 2018

White, Donna L / Hoogeveen, Ron C / Chen, Liang / Richardson, Peter / Ravishankar, Milan / Shah, Preksha / Tinker, Lesley / Rohan, Thomas / Whitsel, Eric A / El-Serag, Hashem B / Jiao, Li. ·Department of Medicine, Baylor College of Medicine, Houston, Texas. · Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael E. DeBakey VA Medical Center, Houston, Texas. · Texas Medical Center Digestive Disease Center, Houston, Texas. · Dan L. Duncan Cancer Center at Baylor College of Medicine, Houston, Texas. · Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey VA Medical Center, Houston, Texas. · Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington. · Albert Einstein College of Medicine, Bronx, New York. · Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. ·Cancer Med · Pubmed #29573228.

ABSTRACT: Advanced glycation end products (AGEs) dysregulate adipokines and induce inflammation by binding to their adipocyte receptor (RAGE). Soluble RAGE (sRAGE) prevents AGEs/RAGE signaling. We performed a nested case-control study of the association between sRAGE, adipokines, and incident pancreatic cancer risk in the prospective Women's Health Initiative Study. We individually matched controls (n = 802) to cases (n = 472) on age, race, and blood draw date. We evaluated serum concentrations of sRAGE, adiponectin, leptin, monocyte chemotactic protein 1 (MCP1), and plasminogen activator inhibitor-1 (PAI1) using immunoassay. We used conditional logistic regression model to estimate adjusted odds ratios (aORs) and 95% confidence intervals (CIs) for pancreatic cancer over biomarker quartiles (Q1-Q4). We used principal component analysis to create two composite biomarkers and performed a confirmatory factor analysis to examine the association between composite biomarker scores (CBS) and pancreatic cancer risk. Baseline serum sRAGE concentrations were inversely associated with pancreatic cancer risk (aOR

5 Article Low-fat Dietary Pattern and Pancreatic Cancer Risk in the Women's Health Initiative Dietary Modification Randomized Controlled Trial. 2018

Jiao, Li / Chen, Liang / White, Donna L / Tinker, Lesley / Chlebowski, Rowan T / Van Horn, Linda V / Richardson, Peter / Lane, Dorothy / Sangi-Haghpeykar, Haleh / El-Serag, Hashem B. ·Department of Medicine, Department of Obstetrics and Gynecology, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX; Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael E. DeBakey VA Medical Center, Houston, TX; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA; Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA; Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Department of Family, Population and Preventive Medicine, Stony Brook University School of Medicine, Stony Brook, NY; Texas Medical Center Digestive Disease Center, Houston, TX; Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey VA Medical Center, Houston, TX; City of Hope National Medical Center, Duarte, CA. ·J Natl Cancer Inst · Pubmed #28922784.

ABSTRACT: Background: Observational studies suggest that diet may influence pancreatic cancer risk. We investigated the effect of a low-fat dietary intervention on pancreatic cancer incidence. Methods: The Women's Health Initiative Dietary Modification (WHI-DM) trial is a randomized controlled trial conducted in 48 835 postmenopausal women age 50 to 79 years in the United States between 1993 and 1998. Women were randomly assigned to the intervention group (n = 19 541), with the goal of reducing total fat intake and increasing intake of vegetables, fruits, and grains, or to the usual diet comparison group (n = 29 294). The intervention concluded in March 2005. We evaluated the effect of the intervention on pancreatic cancer incidence with the follow-up through 2014 using the log-rank test and multivariable Cox proportional hazards regression model. All statistical tests were two-sided. Results: In intention-to-treat analyses including 46 200 women, 92 vs 165 pancreatic cancer cases were ascertained in the intervention vs the comparison group (P = .23). The multivariable hazard ratio (HR) of pancreatic cancer was 0.86 (95% confidence interval [CI] = 0.67 to 1.11). Risk was statistically significantly reduced among women with baseline body mass indexes (BMIs) of 25 kg/m2 or higher (HR = 0.71, 95% CI = 0.53 to 0.96), but not among women with BMIs of less than 25 kg/m2 (HR = 1.62, 95% CI = 0.97 to 2.71, Pinteraction = .01). Conclusions: A low-fat dietary intervention was associated with reduced pancreatic cancer incidence in women who were overweight or obese in the WHI-DM trial. Caution needs to be taken in interpreting the findings based on subgroup analyses.

6 Article Determinants of concentrations of N(ε)-carboxymethyl-lysine and soluble receptor for advanced glycation end products and their associations with risk of pancreatic cancer. 2014

Duan, Zhigang / Chen, Guoqing / Chen, Liang / Stolzenberg-Solomon, Rachael / Weinstein, Stephanie J / Mannisto, Satu / White, Donna L / Albanes, Demetrius / Jiao, Li. ·Department of Medicine, Baylor College of Medicine Houston, TX, USA ; Section of Health Services Research (IQuESt), Michael. E DeBakey VA Medical Center Houston, TX, USA. · Division of Health Services Research, University of Kansas Medical Center Kansas City, KS, USA. · Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health Bethesda, MD, USA. · Department of Chronic Disease Prevention, National Institute for Health and Welfare Helsinki, Finland. · Department of Medicine, Baylor College of Medicine Houston, TX, USA ; Section of Health Services Research (IQuESt), Michael. E DeBakey VA Medical Center Houston, TX, USA ; Texas Medical Center Digestive Disease Center Houston, TX, USA ; Dan L. Duncan Cancer Center at Baylor College of Medicine Houston, TX, USA ; Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey Veterans Affairs Medical Center Houston, TX, USA. ·Int J Mol Epidemiol Genet · Pubmed #25379135.

ABSTRACT: The soluble receptor for advanced glycation end-products (sRAGE) is shown to mitigate pro-inflammatory effects triggered by ligation of RAGE with N(ε)-carboxymethyl-lysine (CML)-AGE or other ligands. We examined the associations among host, lifestyle, and genetic determinants of CML-AGE or sRAGE and risk of pancreatic cancer in the prospective ATBC Study. We obtained baseline exposure information, data on serological and genetic biomarkers from 141 patients with pancreatic cancer and 141 subcohort controls. Stepwise linear and logistic regression models were used for data analysis. Multiple linear regression analyses showed that CML-AGE concentrations were independently inversely correlated with the minor allele of rs640742 of DDOST, physical activity, alcohol consumption, diastolic blood pressure (BP), and positively correlated with heart rate, serum sRAGE and HDL concentrations (P < 0.05). sRAGE concentrations were independently inversely correlated with the 82Ser allele of rs2070600 of RAGE, age, body mass index, heart rate, and serum HDL; and positively correlated with serum CML-AGE, sucrose consumption, and diastolic BP (P < 0.05). The minor allele of rs1035786 of RAGE was associated with reduced risk of pancreatic cancer (any T compared with CC: multivariate OR = 0.61, 95% CI: 0.38-0.98). We identified host metabolic profile, lifestyle and genetic factors that explained approximately 50% of variability of CML-AGE or sRAGE in Finnish men smokers. The association between RAGE SNPs and pancreatic cancer risk warrants further investigation.

7 Article The Healthy Eating Index 2005 and risk for pancreatic cancer in the NIH-AARP study. 2013

Arem, Hannah / Reedy, Jill / Sampson, Josh / Jiao, Li / Hollenbeck, Albert R / Risch, Harvey / Mayne, Susan T / Stolzenberg-Solomon, Rachael Z. ·Yale School of Public Health, New Haven, CT , USA. Aremhe2@mail.nih.gov ·J Natl Cancer Inst · Pubmed #23949329.

ABSTRACT: BACKGROUND: Dietary pattern analyses characterizing combinations of food intakes offer conceptual and statistical advantages over food- and nutrient-based analyses of disease risk. However, few studies have examined dietary patterns and pancreatic cancer risk and none focused on the 2005 Dietary Guidelines for Americans. We used the Healthy Eating Index 2005 (HEI-2005) to estimate the association between meeting those dietary guidelines and pancreatic cancer risk. METHODS: We calculated the HEI-2005 score for 537 218 men and women in the National Institutes of Health-American Association of Retired Persons Diet and Health Study using responses to food frequency questionnaires returned in 1995 and 1996. We used Cox proportional hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for risk of pancreatic cancer according to HEI-2005 quintiles and explored effect modification by known risk factors. P interaction values were calculated using the Wald test. All statistical tests were two-sided. RESULTS: We identified 2383 incident, exocrine pancreatic cancer cases (median = 10.5 years follow-up). Comparing participants who met the most dietary guidelines (Q5) with those who met the fewest guidelines (Q1), we observed a reduced risk of pancreatic cancer (HR = 0.85, 95% CI = 0.74 to 0.97). Among men there was an interaction by body mass index (P interaction = .03), with a hazard ratio of 0.72 (95% CI = 0.59 to 0.88) comparing Q5 vs Q1 in overweight/obese men (body mass index ≥ 25 kg/m(2)) but no association among normal weight men. CONCLUSIONS: Our findings support the hypothesis that consuming a high-quality diet, as scored by the HEI-2005, may reduce the risk of pancreatic cancer.

8 Article Inflammatory plasma markers and pancreatic cancer risk: a prospective study of five U.S. cohorts. 2013

Bao, Ying / Giovannucci, Edward L / Kraft, Peter / Qian, Zhi Rong / Wu, Chen / Ogino, Shuji / Gaziano, J Michael / Stampfer, Meir J / Ma, Jing / Buring, Julie E / Sesso, Howard D / Lee, I-Min / Rifai, Nader / Pollak, Michael N / Jiao, Li / Lessin, Lawrence / Cochrane, Barbara B / Manson, Joann E / Fuchs, Charles S / Wolpin, Brian M. ·Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA. ying.bao@channing.harvard.edu ·Cancer Epidemiol Biomarkers Prev · Pubmed #23462920.

ABSTRACT: Chronic inflammation may play a role in the development of pancreatic cancer. However, few prospective studies have examined the association between plasma inflammatory markers and pancreatic cancer risk. Therefore, we investigated the association of prediagnostic circulating C-reactive protein (CRP), interleukin-6 (IL-6), and TNF-α receptor II (TNF-αR2) with subsequent pancreatic cancer risk in a prospective, nested case-control study of 470 cases and 1,094 controls from Health Professionals Follow-up Study, Nurses' Health Study, Physicians' Health Study, Women's Health Initiative, and Women's Health Study. The median follow-up time of cases was 7.2 years (range 1-26 years). No association was observed between plasma CRP, IL-6, and TNF-αR2 and the risk of pancreatic cancer. Comparing extreme quintiles, the multivariate ORs were 1.10 [95% confidence interval (CI), 0.74-1.63; Ptrend = 0.81] for CRP, 1.19 (95% CI, 0.81-1.76; Ptrend = 0.08) for IL-6, and 0.88 (95% CI, 0.58-1.33; Ptrend = 0.57) for TNF-αR2. In conclusion, prediagnostic levels of circulating CRP, IL-6, and TNF-αR2 were not associated with the risk of pancreatic cancer, suggesting that systemic inflammation as measured by circulating inflammatory factors is unlikely to play a major role in the development of pancreatic cancer.

9 Article Pathway analysis of genome-wide association study data highlights pancreatic development genes as susceptibility factors for pancreatic cancer. 2012

Li, Donghui / Duell, Eric J / Yu, Kai / Risch, Harvey A / Olson, Sara H / Kooperberg, Charles / Wolpin, Brian M / Jiao, Li / Dong, Xiaoqun / Wheeler, Bill / Arslan, Alan A / Bueno-de-Mesquita, H Bas / Fuchs, Charles S / Gallinger, Steven / Gross, Myron / Hartge, Patricia / Hoover, Robert N / Holly, Elizabeth A / Jacobs, Eric J / Klein, Alison P / LaCroix, Andrea / Mandelson, Margaret T / Petersen, Gloria / Zheng, Wei / Agalliu, Ilir / Albanes, Demetrius / Boutron-Ruault, Marie-Christine / Bracci, Paige M / Buring, Julie E / Canzian, Federico / Chang, Kenneth / Chanock, Stephen J / Cotterchio, Michelle / Gaziano, J Michael / Giovannucci, Edward L / Goggins, Michael / Hallmans, Göran / Hankinson, Susan E / Hoffman Bolton, Judith A / Hunter, David J / Hutchinson, Amy / Jacobs, Kevin B / Jenab, Mazda / Khaw, Kay-Tee / Kraft, Peter / Krogh, Vittorio / Kurtz, Robert C / McWilliams, Robert R / Mendelsohn, Julie B / Patel, Alpa V / Rabe, Kari G / Riboli, Elio / Shu, Xiao-Ou / Tjønneland, Anne / Tobias, Geoffrey S / Trichopoulos, Dimitrios / Virtamo, Jarmo / Visvanathan, Kala / Watters, Joanne / Yu, Herbert / Zeleniuch-Jacquotte, Anne / Amundadottir, Laufey / Stolzenberg-Solomon, Rachael Z. ·Department of Gastrointestinal Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA. ·Carcinogenesis · Pubmed #22523087.

ABSTRACT: Four loci have been associated with pancreatic cancer through genome-wide association studies (GWAS). Pathway-based analysis of GWAS data is a complementary approach to identify groups of genes or biological pathways enriched with disease-associated single-nucleotide polymorphisms (SNPs) whose individual effect sizes may be too small to be detected by standard single-locus methods. We used the adaptive rank truncated product method in a pathway-based analysis of GWAS data from 3851 pancreatic cancer cases and 3934 control participants pooled from 12 cohort studies and 8 case-control studies (PanScan). We compiled 23 biological pathways hypothesized to be relevant to pancreatic cancer and observed a nominal association between pancreatic cancer and five pathways (P < 0.05), i.e. pancreatic development, Helicobacter pylori lacto/neolacto, hedgehog, Th1/Th2 immune response and apoptosis (P = 2.0 × 10(-6), 1.6 × 10(-5), 0.0019, 0.019 and 0.023, respectively). After excluding previously identified genes from the original GWAS in three pathways (NR5A2, ABO and SHH), the pancreatic development pathway remained significant (P = 8.3 × 10(-5)), whereas the others did not. The most significant genes (P < 0.01) in the five pathways were NR5A2, HNF1A, HNF4G and PDX1 for pancreatic development; ABO for H.pylori lacto/neolacto; SHH for hedgehog; TGFBR2 and CCL18 for Th1/Th2 immune response and MAPK8 and BCL2L11 for apoptosis. Our results provide a link between inherited variation in genes important for pancreatic development and cancer and show that pathway-based approaches to analysis of GWAS data can yield important insights into the collective role of genetic risk variants in cancer.

10 Article Evidence that serum levels of the soluble receptor for advanced glycation end products are inversely associated with pancreatic cancer risk: a prospective study. 2011

Jiao, Li / Weinstein, Stephanie J / Albanes, Demetrius / Taylor, Philip R / Graubard, Barry I / Virtamo, Jarmo / Stolzenberg-Solomon, Rachael Z. ·Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. jiao@bcm.edu ·Cancer Res · Pubmed #21540233.

ABSTRACT: Cigarette smoking, obesity, type 2 diabetes, and, to a lesser extent, meat cooked at high temperatures are associated with pancreatic cancer. Cigarette smoke and foods cooked at higher temperatures are major environmental sources of advanced glycation end products (AGE). AGEs accumulate during hyperglycemia and elicit oxidative stress and inflammation through interaction with the receptor for AGEs (RAGE). Soluble RAGE (sRAGE) acts as an anti-inflammatory factor to neutralize AGEs and block the effects mediated by RAGE. In this study, we investigated the associations of prediagnostic measures of N(ε)-(carboxymethyl)-lysine (CML)-AGE and sRAGE with pancreatic cancer in a case-cohort study within a cohort of 29,133 Finnish male smokers. Serum samples and exposure information were collected at baseline (1985-1988). We measured CML-AGE, sRAGE, glucose, and insulin concentrations in fasting serum from 255 incident pancreatic cancer cases that arose through April 2005 and from 485 randomly sampled subcohort participants. Weighted Cox proportional hazard regression models were used to calculate relative risks (RR) and 95% CI, adjusted for age, years of smoking, and body mass index. CML-AGE and sRAGE were mutually adjusted. CML-AGE levels were not associated with pancreatic cancer [fifth compared with first quintile, RR (95% CI): 0.68 (0.38-1.22), P(trend) = 0.27]. In contrast, sRAGE levels were inversely associated with pancreatic cancer [fifth compared with first quintile, RR (95% CI): 0.46 (0.23-0.73), P(trend) = 0.002]. Further adjustment for glucose or insulin levels did not change the observed associations. Our findings suggest that sRAGE is inversely associated with pancreatic cancer risk among Finnish male smokers.

11 Article Available carbohydrates, glycemic load, and pancreatic cancer: is there a link? 2010

Meinhold, Cari L / Dodd, Kevin W / Jiao, Li / Flood, Andrew / Shikany, James M / Genkinger, Jeanine M / Hayes, Richard B / Stolzenberg-Solomon, Rachael Z. ·National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland 20852, USA. ·Am J Epidemiol · Pubmed #20452999.

ABSTRACT: High-carbohydrate diets have been linked to pancreatic cancer risk in case-control studies, but prospective studies have shown mostly null results. The authors investigated the associations of glycemic load, glycemic index, and carbohydrate intake with pancreatic cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Dietary intake was assessed by using a self-administered questionnaire. Between 1998 and 2006 (median follow-up = 6.5 years), 266 incident, confirmed pancreatic cancers were identified among 109,175 participants. Hazards ratios and 95% confidence intervals were adjusted for sex, smoking, body mass index, and total energy. Overall, elevated risks for pancreatic cancer were observed in the 90th versus 10th percentile of glycemic load (hazards ratio (HR) = 1.45, 95% confidence interval (CI): 1.05, 2.00), available carbohydrate (HR = 1.47, 95% CI: 1.05, 2.06), and sucrose (HR = 1.37, 95% CI: 0.99, 1.89) intake. The positive association for available carbohydrate intake was observed during the first 4 years of follow-up (HR(<2 years) = 2.60, 95% CI: 1.34, 5.06; HR(2-<4 years) = 1.94, 95% CI: 1.06, 3.55) but not subsequently (HR = 0.86, 95% CI: 0.52, 1.44); the opposite pattern was observed for total fat and saturated fat intake. Rather than being causal, the short-term increase in pancreatic cancer risk associated with high available carbohydrate and low fat intake may be capturing dietary changes associated with subclinical disease.

12 Article Body mass index, effect modifiers, and risk of pancreatic cancer: a pooled study of seven prospective cohorts. 2010

Jiao, Li / Berrington de Gonzalez, Amy / Hartge, Patricia / Pfeiffer, Ruth M / Park, Yikyung / Freedman, D Michal / Gail, Mitchell H / Alavanja, Michael C R / Albanes, Demetrius / Beane Freeman, Laura E / Chow, Wong-Ho / Huang, Wen-Yi / Hayes, Richard B / Hoppin, Jane A / Ji, Bu-Tian / Leitzmann, Michael F / Linet, Martha S / Meinhold, Cari L / Schairer, Catherine / Schatzkin, Arthur / Virtamo, Jarmo / Weinstein, Stephanie J / Zheng, Wei / Stolzenberg-Solomon, Rachael Z. ·Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. jiao@bcm.edu ·Cancer Causes Control · Pubmed #20383573.

ABSTRACT: OBJECTIVE: To investigate whether the positive association of body mass index (BMI, kg/m(2)) with risk of pancreatic cancer is modified by age, sex, smoking status, physical activity, and history of diabetes. METHODS: In a pooled analysis of primary data of seven prospective cohorts including 458,070 men and 485,689 women, we identified 2,454 patients with incident pancreatic cancer during an average 6.9 years of follow-up. Cox proportional hazard regression models were used in data analysis. RESULTS: In a random-effects meta-analysis, for every 5 kg/m(2) increment in BMI, the summary relative risk (RR) was 1.06 (95% confidence interval (CI) 0.99-1.13) for men and 1.12 (95% CI 1.05-1.19) for women. The aggregate analysis showed that compared with normal weight (BMI: 18.5 to <25), the adjusted RR was 1.13 (95% CI 1.03-1.23) for overweight (BMI: 25 to <30) and 1.19 (95% CI 1.05-1.35) for obesity class I (BMI: 30 to <35). Tests of interactions of BMI effects by other risk factors were not statistically significant. Every 5 kg/m(2) increment in BMI was associated with an increased risk of pancreatic cancer among never and former smokers, but not among current smokers (P-interaction = 0.08). CONCLUSION: The present evidence suggests that a high BMI is an independent risk factor of pancreatic cancer.

13 Article Alcohol intake and pancreatic cancer: a pooled analysis from the pancreatic cancer cohort consortium (PanScan). 2010

Michaud, Dominique S / Vrieling, Alina / Jiao, Li / Mendelsohn, Julie B / Steplowski, Emily / Lynch, Shannon M / Wactawski-Wende, Jean / Arslan, Alan A / Bas Bueno-de-Mesquita, H / Fuchs, Charles S / Gross, Myron / Helzlsouer, Kathy / Jacobs, Eric J / Lacroix, Andrea / Petersen, Gloria / Zheng, Wei / Allen, Naomi / Ammundadottir, Laufey / Bergmann, Manuela M / Boffetta, Paolo / Buring, Julie E / Canzian, Federico / Chanock, Stephen J / Clavel-Chapelon, Françoise / Clipp, Sandra / Freiberg, Matthew S / Michael Gaziano, J / Giovannucci, Edward L / Hankinson, Susan / Hartge, Patricia / Hoover, Robert N / Allan Hubbell, F / Hunter, David J / Hutchinson, Amy / Jacobs, Kevin / Kooperberg, Charles / Kraft, Peter / Manjer, Jonas / Navarro, Carmen / Peeters, Petra H M / Shu, Xiao-Ou / Stevens, Victoria / Thomas, Gilles / Tjønneland, Anne / Tobias, Geoffrey S / Trichopoulos, Dimitrios / Tumino, Rosario / Vineis, Paolo / Virtamo, Jarmo / Wallace, Robert / Wolpin, Brian M / Yu, Kai / Zeleniuch-Jacquotte, Anne / Stolzenberg-Solomon, Rachael Z. ·Division of Epidemiology, Public Health and Primary Care, Imperial College London, London, UK. d.michaud@imperial.ac.uk ·Cancer Causes Control · Pubmed #20373013.

ABSTRACT: The literature has consistently reported no association between low to moderate alcohol consumption and pancreatic cancer; however, a few studies have shown that high levels of intake may increase risk. Most single studies have limited power to detect associations even in the highest alcohol intake categories or to examine associations by alcohol type. We analyzed these associations using 1,530 pancreatic cancer cases and 1,530 controls from the Pancreatic Cancer Cohort Consortium (PanScan) nested case-control study. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using unconditional logistic regression, adjusting for potential confounders. We observed no significant overall association between total alcohol (ethanol) intake and pancreatic cancer risk (OR = 1.38, 95% CI = 0.86-2.23, for 60 or more g/day vs. >0 to <5 g/day). A statistically significant increase in risk was observed among men consuming 45 or more grams of alcohol from liquor per day (OR = 2.23, 95% CI = 1.02-4.87, compared to 0 g/day of alcohol from liquor, P-trend = 0.12), but not among women (OR = 1.35, 95% CI = 0.63-2.87, for 30 or more g/day of alcohol from liquor, compared to none). No associations were noted for wine or beer intake. Overall, no significant increase in risk was observed, but a small effect among heavy drinkers cannot be ruled out.