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Pancreatic Neoplasms: HELP
Articles from National Cancer Institute Rockville
Based on 45 articles published since 2010
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These are the 45 published articles about Pancreatic Neoplasms that originated from National Cancer Institute Rockville during 2010-2020.
 
+ Citations + Abstracts
Pages: 1 · 2
1 Editorial Pancreatic Cancer Chemoprevention: Challenges and Opportunities. 2018

Mohammed, Altaf / Rao, Chinthalapally V. ·Chemopreventive Agent Development Research Group (CADRG) Division of Cancer Prevention National Cancer Institute Rockville, MD 20850, United States. · Center for Cancer Prevention and Drug Development (CCPDD) Stephenson Cancer Center, Medical Oncology University of Oklahoma Health Sciences Center Oklahoma City, OK 73104, United States. ·Curr Med Chem · Pubmed #30014794.

ABSTRACT: -- No abstract --

2 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.

3 Review Detecting circulating tumor material and digital pathology imaging during pancreatic cancer progression. 2017

Moravec, Radim / Divi, Rao / Verma, Mukesh. ·Radim Moravec, Surveillance Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health, Rockville, MD 20850, United States. ·World J Gastrointest Oncol · Pubmed #28656074.

ABSTRACT: Pancreatic cancer (PC) is a leading cause of cancer-related death worldwide. Clinical symptoms typically present late when treatment options are limited and survival expectancy is very short. Metastatic mutations are heterogeneous and can accumulate up to twenty years before PC diagnosis. Given such genetic diversity, detecting and managing the complex states of disease progression may be limited to imaging modalities and markers present in circulation. Recent developments in digital pathology imaging show potential for early PC detection, making a differential diagnosis, and predicting treatment sensitivity leading to long-term survival in advanced stage patients. Despite large research efforts, the only serum marker currently approved for clinical use is CA 19-9. Utility of CA 19-9 has been shown to improve when it is used in combination with PC-specific markers. Efforts are being made to develop early-screening assays that can detect tumor-derived material, present in circulation, before metastasis takes a significant course. Detection of markers that identify circulating tumor cells and tumor-derived extracellular vesicles (EVs) in biofluid samples offers a promising non-invasive method for this purpose. Circulating tumor cells exhibit varying expression of epithelial and mesenchymal markers depending on the state of tumor differentiation. This offers a possibility for monitoring disease progression using minimally invasive procedures. EVs also offer the benefit of detecting molecular cargo of tumor origin and add the potential to detect circulating vesicle markers from tumors that lack invasive properties. This review integrates recent genetic insights of PC progression with developments in digital pathology and early detection of tumor-derived circulating material.

4 Review Potential usefulness of apolipoprotein A2 isoforms for screening and risk stratification of pancreatic cancer. 2016

Honda, Kazufumi / Srivastava, Sudhir. ·Division of Chemotherapy & Clinical Research, National Cancer Center Research Institute, Tokyo 104-0045, Japan. · Japan Agency for Medical Research & Development (AMED) CREST, Tokyo 100-0004, Japan. · Division of Cancer Prevention, National Cancer Institute, Rockville, MD 20852, USA. ·Biomark Med · Pubmed #27673558.

ABSTRACT: Given the low incidence of pancreatic cancer in the general population, screening of pancreatic cancer in the general population using invasive modalities is not feasible. Combination of invasive screening with noninvasive biomarkers for pancreatic cancer and its precancerous lesions has the potential to reduce mortality due to pancreatic cancer. In this review, we focus on biomarkers found in the blood that can indicate early-stage pancreatic cancer, and we discuss current strategies for screening for pancreatic cancer. We recently identified a unique alteration in apolipoprotein A2 isoforms in pancreatic cancer and its precancerous lesions, and we describe its clinical usefulness as a potential biomarker for the early detection and risk stratification of pancreatic cancer.

5 Review Targeting the microenvironment of pancreatic cancer: overcoming treatment barriers and improving local immune responses. 2016

Strauss, J / Alewine, C / Figg, W D / Duffy, A. ·NCI/NIH, 9000 Rockville Pike, Bldg 10/Room 12 N-226, Bethesda, MD, 20892, USA. julius.strauss@nih.gov. · NCI/NIH, 9000 Rockville Pike, Building 37, Room 5116B, Bethesda, MD, 20892, USA. · NCI/NIH, 9000 Rockville Pike, Bldg 10/Room 5A-01, Bethesda, MD, 20892, USA. · NCI/NIH, 9000 Rockville Pike, Bldg 10/Room 12 N-226, Bethesda, MD, 20892, USA. ·Clin Transl Oncol · Pubmed #26661112.

ABSTRACT: Historically, patients diagnosed with metastatic pancreatic cancer have faced a grim prognosis. The survival benefit seen with systemic chemotherapies and even combinations thereof have been disappointing. However, growing data suggest that the microenvironment of pancreatic cancer may be contributing to this poor prognosis. This microenvironment has a dense fibrotic stroma, and is hypoxic and highly immunosuppressive, all of which pose barriers to treatment. Newer strategies looking to disrupt the fibrotic stroma, target hypoxic areas, and improve local immune responses in the tumor microenvironment are currently undergoing clinical evaluation and seem to offer great promise. In addition to these therapies, preclinical work evaluating novel cytotoxic agents including nanoparticles has also been encouraging. While much research still needs to be done, these strategies offer new hope for patients with pancreatic cancer.

6 Review Epidemiology and Inherited Predisposition for Sporadic Pancreatic Adenocarcinoma. 2015

Stolzenberg-Solomon, Rachael Z / Amundadottir, Laufey T. ·Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 9609 Medical Center Drive, Room 6E420, Rockville, MD 20850, USA. Electronic address: rs221z@nih.gov. · Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 8717 Grovemont Circle, Bethesda, MD 20892, USA. Electronic address: amundadottirl@mail.nih.gov. ·Hematol Oncol Clin North Am · Pubmed #26226901.

ABSTRACT: Given the changing demographics of Western populations, the numbers of pancreatic cancer cases are projected to increase during the next decade. Diabetes, recent cigarette smoking, and excess body weight are the cancer's most consistent risk factors. The search for common and rare germline variants that influence risk of pancreatic cancer through genome-wide association studies and high-throughput-sequencing-based studies is underway and holds the promise of increasing the knowledge of variants and genes that play a role in inherited susceptibility of this disease. Research reported in this review has advanced the understanding of pancreatic cancer.

7 Review Early detection of sporadic pancreatic cancer: summative review. 2015

Chari, Suresh T / Kelly, Kimberly / Hollingsworth, Michael A / Thayer, Sarah P / Ahlquist, David A / Andersen, Dana K / Batra, Surinder K / Brentnall, Teresa A / Canto, Marcia / Cleeter, Deborah F / Firpo, Matthew A / Gambhir, Sanjiv Sam / Go, Vay Liang W / Hines, O Joe / Kenner, Barbara J / Klimstra, David S / Lerch, Markus M / Levy, Michael J / Maitra, Anirban / Mulvihill, Sean J / Petersen, Gloria M / Rhim, Andrew D / Simeone, Diane M / Srivastava, Sudhir / Tanaka, Masao / Vinik, Aaron I / Wong, David. ·From the *Department of Medicine, Mayo Clinic, Rochester, MN; †Department of Biomedical Engineering, University of Virginia, Charlottesville, VA; Departments of ‡Biochemistry and Molecular Biology, §Pathology and Microbiology, and ∥Surgery, Fred & Pamela Buffett Cancer Center, University of Nebraska, Omaha, NE; ¶Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Disease, National Institutes of Health, Bethesda, MD; #Division of Gastroenterology, University of Washington, Seattle, WA; **Division of Gastroenterology, Johns Hopkins University School of Medicine, Baltimore, MD; ††Sawgrass Leadership Institute, Ponte Vedra Beach, FL; ‡‡Department of Surgery, University of Utah, Salt Lake City, UT; §§Department of Radiology, Stanford University School of Medicine, Stanford; ∥∥Department of Medicine, David Geffen School of Medicine, and ¶¶General Surgery, University of California Los Angeles, Los Angeles, CA; ##Kenner Family Research Fund; ***Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY; †††Department of Internal Medicine, University of Greifswald, Greifswald, Germany; ‡‡‡Division of Pathology and Laboratory Medicine, University of Texas MD Anderson Cancer Center, Houston, TX; §§§Department of Health Sciences Research, Mayo Clinic, Rochester, MN; ∥∥∥Gastroenterology Division, Department of Internal Medicine and Comprehensive Cancer Center, and ¶¶¶Department of Surgery, School of Medicine, University of Michigan, Ann Arbor, MI; ###Cancer Biomarkers Research Group, Division of Cancer Prevention, National Cancer Institute, Rockville, MD; ****Departments of Surgery and Oncology, Kyushu University, Fukuoka, Japan; ††††Department of Medicine, Eastern Virginia Medical School, Norfolk, VA; and ‡‡‡‡Division of Oral Biology and Medicine, CLA School of Dentistry, Jonnson Comprehensive Cancer Center, University of California Los Angeles, L ·Pancreas · Pubmed #25931254.

ABSTRACT: Pancreatic cancer (PC) is estimated to become the second leading cause of cancer death in the United States by 2020. Early detection is the key to improving survival in PC. Addressing this urgent need, the Kenner Family Research Fund conducted the inaugural Early Detection of Sporadic Pancreatic Cancer Summit Conference in 2014 in conjunction with the 45th Anniversary Meeting of the American Pancreatic Association and Japan Pancreas Society. This seminal convening of international representatives from science, practice, and clinical research was designed to facilitate challenging interdisciplinary conversations to generate innovative ideas leading to the creation of a defined collaborative strategic pathway for the future of the field. An in-depth summary of current efforts in the field, analysis of gaps in specific areas of expertise, and challenges that exist in early detection is presented within distinct areas of inquiry: Case for Early Detection: Definitions, Detection, Survival, and Challenges; Biomarkers for Early Detection; Imaging; and Collaborative Studies. In addition, an overview of efforts in familial PC is presented in an addendum to this article. It is clear from the summit deliberations that only strategically designed collaboration among investigators, institutions, and funders will lead to significant progress in early detection of sporadic PC.

8 Clinical Trial Randomized Phase 2 Trial of the Oncolytic Virus Pelareorep (Reolysin) in Upfront Treatment of Metastatic Pancreatic Adenocarcinoma. 2016

Noonan, Anne M / Farren, Matthew R / Geyer, Susan M / Huang, Ying / Tahiri, Sanaa / Ahn, Daniel / Mikhail, Sameh / Ciombor, Kristen K / Pant, Shubham / Aparo, Santiago / Sexton, Jennifer / Marshall, John L / Mace, Thomas A / Wu, Christina S / El-Rayes, Bassel / Timmers, Cynthia D / Zwiebel, James / Lesinski, Gregory B / Villalona-Calero, Miguel A / Bekaii-Saab, Tanios S. ·Department of Internal Medicine, Division of Medical Oncology, The Ohio State University, Columbus, Ohio, USA. · Health Informatics Institute, University of South Florida, Tampa, Florida, USA. · Department of Medicine, Hematology/Oncology, Oklahoma University Cancer Institute, Oklahoma City, Oklahoma, USA. · Department of Medical Oncology, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York, USA. · Georgetown Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, District of Columbia, USA. · Department of Medical Oncology, Winship Cancer Institute, Emory University, Atlanta, Georgia, USA. · Solid Tumor Translational Science Shared Resource, The James Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, USA. · Investigational Drug Branch, Cancer Therapy Evaluation Program, National Cancer Institute, Rockville, Maryland, USA. · Department of Internal Medicine, Division of Medical Oncology, The Ohio State University, Columbus, Ohio, USA. Electronic address: Bekaii-Saab.tanios@mayo.edu. ·Mol Ther · Pubmed #27039845.

ABSTRACT: Pelareorep causes oncolysis in tumor cells with activated Ras. We hypothesized that pelareorep would have efficacy and immunomodulatory activity in metastatic pancreatic adenocarcinoma (MPA) when combined with carboplatin and paclitaxel. A randomized phase 2 study (NCT01280058) was conducted in treatment-naive patients with MPA randomized to two treatment arms: paclitaxel/carboplatin + pelareorep (Arm A, n = 36 evaluable patients) versus paclitaxel/carboplatin (Arm B, n = 37 evaluable patients). There was no difference in progression-free survival (PFS) between the arms (Arm A PFS = 4.9 months, Arm B PFS = 5.2 months, P = 0.6), and Kirsten rat sarcoma viral oncogene (KRAS) status did not impact outcome. Quality-adjusted Time without Symptoms or Toxicity analysis revealed that the majority of PFS time was without toxicity or progression (4.3 months). Patient immunophenotype appeared important, as soluble immune biomarkers were associated with treatment outcome (fractalkine, interleukin (IL)-6, IL-8, regulated on activation, normal T cell expressed and secreted (RANTES), and vascular endothelial growth factor (VEGF)). Increased circulating T and natural killer (NK)-cell subsets were also significantly associated with treatment outcome. Addition of pelareorep was associated with higher levels of 14 proinflammatory plasma cytokines/chemokines and cells with an immunosuppressive phenotype (Tregs, cytotoxic T lymphocyte associated protein 4 (CTLA4)(+) T cells). Overall, pelareorep was safe but does not improve PFS when administered with carboplatin/paclitaxel, regardless of KRAS mutational status. Immunologic studies suggest that chemotherapy backbone improves immune reconstitution and that targeting remaining immunosuppressive mediators may improve oncolytic virotherapy.

9 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.

10 Clinical Trial Multicenter Phase II Trial of Temsirolimus and Bevacizumab in Pancreatic Neuroendocrine Tumors. 2015

Hobday, Timothy J / Qin, Rui / Reidy-Lagunes, Diane / Moore, Malcolm J / Strosberg, Jonathan / Kaubisch, Andreas / Shah, Manisha / Kindler, Hedy Lee / Lenz, Heinz-Josef / Chen, Helen / Erlichman, Charles. ·Timothy J. Hobday, Rui Qin, and Charles Erlichman, Mayo Clinic, Rochester, MN · Diane Reidy-Lagunes, Memorial Sloan Kettering Cancer Center, New York · Andreas Kaubisch, Montefiore Medical Center, Bronx, NY · Malcolm J. Moore, Princess Margaret Hospital, Toronto, Ontario, Canada · Jonathan Strosberg, H. Lee Moffitt Cancer Center, Tampa, FL · Manisha Shah, Ohio State University, Columbus, OH · Hedy Lee Kindler, University of Chicago, Chicago, IL · Heinz-Josef Lenz, University of Southern California, Los Angeles, CA · and Helen Chen, National Cancer Institute, Rockville, MD. ·J Clin Oncol · Pubmed #25488966.

ABSTRACT: PURPOSE: There are few effective therapies for pancreatic neuroendocrine tumors (PNETs). Recent placebo-controlled phase III trials of the mammalian target of rapamycin (mTOR) inhibitor everolimus and the vascular endothelial growth factor (VEGF)/platelet-derived growth factor receptor inhibitor sunitinib have noted improved progression-free survival (PFS). Preclinical studies have suggested enhanced antitumor effects with combined mTOR and VEGF pathway-targeted therapy. We conducted a clinical trial to evaluate combination therapy against these targets in PNETs. PATIENTS AND METHODS: We conducted a two-stage single-arm phase II trial of the mTOR inhibitor temsirolimus 25 mg intravenously (IV) once per week and the VEGF-A monoclonal antibody bevacizumab 10 mg/kg IV once every 2 weeks in patients with well or moderately differentiated PNETs and progressive disease by RECIST within 7 months of study entry. Coprimary end points were tumor response rate and 6-month PFS. RESULTS: A total of 58 patients were enrolled, and 56 patients were eligible for response assessment. Confirmed response rate (RR) was 41% (23 of 56 patients). PFS at 6 months was 79% (44 of 56). Median PFS was 13.2 months (95% CI, 11.2 to 16.6). Median overall survival was 34 months (95% CI, 27.1 to not reached). For evaluable patients, the most common grade 3 to 4 adverse events attributed to therapy were hypertension (21%), fatigue (16%), lymphopenia (14%), and hyperglycemia (14%). CONCLUSION: The combination of temsirolimus and bevacizumab had substantial activity and reasonable tolerability in a multicenter phase II trial, with RR of 41%, well in excess of single targeted agents in patients with progressive PNETs. Six-month PFS was a notable 79% in a population of patients with disease progression by RECIST criteria within 7 months of study entry. On the basis of this trial, continued evaluation of combination mTOR and VEGF pathway inhibitors is warranted.

11 Article Radiation and Risk of Liver, Biliary Tract, and Pancreatic Cancers among Atomic Bomb Survivors in Hiroshima and Nagasaki: 1958-2009. 2019

Sadakane, Atsuko / French, Benjamin / Brenner, Alina V / Preston, Dale L / Sugiyama, Hiromi / Grant, Eric J / Sakata, Ritsu / Utada, Mai / Cahoon, Elizabeth K / Mabuchi, Kiyohiko / Ozasa, Kotaro. ·Departments of Epidemiology. · Departments of Statistics. · Departments of Hirosoft International Corporation, Eureka, California. · Departments of Associate Chief of Research, Radiation Effects Research Foundation, Hiroshima, Japan. · Departments of Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland. ·Radiat Res · Pubmed #31291162.

ABSTRACT: The Life Span Study (LSS) of atomic bomb survivors has consistently demonstrated significant excess radiation-related risks of liver cancer since the first cancer incidence report. Here, we present updated information on radiation risks of liver, biliary tract and pancreatic cancers based on 11 additional years of follow-up since the last report, from 1958 to 2009. The current analyses used improved individual radiation doses and accounted for the effects of alcohol consumption, smoking and body mass index. The study participants included 105,444 LSS participants with known individual radiation dose and no known history of cancer at the start of follow-up. Cases were the first primary incident cancers of the liver (including intrahepatic bile duct), biliary tract (gallbladder and other and unspecified parts of biliary tract) or pancreas identified through linkage with population-based cancer registries in Hiroshima and Nagasaki. Poisson regression methods were used to estimate excess relative risks (ERRs) and excess absolute risks (EARs) associated with DS02R1 doses for liver (liver and biliary tract cancers) or pancreas (pancreatic cancer). We identified 2,016 incident liver cancer cases during the follow-up period. Radiation dose was significantly associated with liver cancer risk (ERR per Gy: 0.53, 95% CI: 0.23 to 0.89; EAR per 10,000 person-year Gy: 5.32, 95% CI: 2.49 to 8.51). There was no evidence for curvature in the radiation dose response (

12 Article Serum selenium and pancreatic cancer: a prospective study in the Prostate, Lung, Colorectal and Ovarian Cancer Trial cohort. 2019

Chatterjee, Sharmila / Combs, Gerald F / Chattopadhyay, Amit / Stolzenberg-Solomon, Rachael. ·Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Rockville, MD, 20850, USA. sharmilahotmail@hotmail.com. · Grand Forks Human Nutrition Research Center, 2420 2nd Ave N, ARS/USDA, Grand Forks, ND, 58203, USA. · School of Dental Medicine, Case Western Reserve University, Cleveland, OH, 44106, USA. · La Trobe, La Trobe University Rural Health School, Melbourne, Australia. · Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Rockville, MD, 20850, USA. rs221z@nih.gov. ·Cancer Causes Control · Pubmed #30915619.

ABSTRACT: PURPOSE: Pancreatic cancer(PCa) is one of the most lethal cancers with few known consistent nutrition-related risk factors. Epidemiologic associations between the trace element selenium and PCa are inconsistent. This study examined the association of pre-diagnostic serum selenium with incident PCa. METHODS: We conducted a nested case-control study within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Study (PLCO) cohort of men and women 55-70 years old at baseline (1993-2001). In total, 303 PCa cases developed during the 17-year follow-up period (1993-2009). We selected two controls (n = 606) for each case who were alive at the time the case was diagnosed who were matched on age, sex, race, and date of blood draw. We used conditional logistic regression analysis to calculate the odds ratio (OR) and 95% confidence intervals (CI) adjusting for smoking status and diabetes mellitus. RESULTS: Mean serum selenium concentrations were slightly lower in cases (mean, 95% CI: 139.0 ng/ml, 135.6-138.9) compared to controls (142.5 ng/ml, 140.4-142.4, p = 0.08). Overall, serum selenium was not associated with PCa risk (continuous OR: 0.66; 0.32-1.37). There was no significant interaction by sex, smoking, diabetes, or follow-up time (p > 0.05). CONCLUSION: Our results do not support the hypothesis that serum selenium is associated with PCa risk.

13 Article A Prospective Study to Establish a New-Onset Diabetes Cohort: From the Consortium for the Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer. 2018

Maitra, Anirban / Sharma, Ayush / Brand, Randall E / Van Den Eeden, Stephen K / Fisher, William E / Hart, Phil A / Hughes, Steven J / Mather, Kieren J / Pandol, Stephen J / Park, Walter G / Feng, Ziding / Serrano, Jose / Rinaudo, Jo Ann S / Srivastava, Sudhir / Chari, Suresh T / Anonymous3720965. ·Division of Gastroenterology, Department of Medicine, Mayo Clinic, Rochester, MN. · Division of Gastroenterology, University of Pittsburgh Medical Center, Pittsburgh, PA. · Division of Research, Kaiser Permanente Northern California, Oakland, CA. · Division of Gastroenterology, Baylor College of Medicine, Houston, TX. · Division of Gastroenterology, The Ohio State University Wexner Medical Center, Columbus, OH. · Department of Surgery, College of Medicine, University of Florida Health Science Center, Gainesville, FL. · Division of Endocrinology and Metabolism, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN. · Division of Gastroenterology, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, CA. · Division of Gastroenterology and Hepatology, Stanford University Medical Center, Stanford, CA. · Department of Biostatistics, Fred Hutchinson Cancer Research Center, Seattle, WA. · Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD. · Division of Cancer Prevention, National Cancer Institute, Rockville, MD. ·Pancreas · Pubmed #30325864.

ABSTRACT: The National Cancer Institute and the National Institute for Diabetes and Digestive and Kidney Diseases initiated the Consortium for the Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer (CPDPC) in 2015 (the CPDPC's origin, structure, governance, and research objectives are described in another article in this journal). One of the key objectives of CPDPC is to assemble a cohort of 10,000 subjects 50 years or older with new-onset diabetes, called the NOD cohort. Using a define, enrich, and find early detection approach, the aims of the NOD study are to (a) estimate the 3-year probability of pancreatic ductal adenocarcinoma (PDAC) in NOD (define), (b) establish a biobank of clinically annotated biospecimens from presymptomatic PDAC and control new-onset type 2 diabetes mellitus subjects, (c) conduct phase 3 validation studies of promising biomarkers for identification of incident PDAC in NOD patients (enrich), and (d) provide a platform for development of a future interventional screening protocol for early detection of PDAC in patients with NOD that incorporates imaging studies and/or clinical algorithms (find). It is expected that 85 to 100 incidences of PDAC will be diagnosed during the study period in this cohort of 10,000 patients.

14 Article Evaluation of a Mixed Meal Test for Diagnosis and Characterization of PancrEaTogEniC DiabeTes Secondary to Pancreatic Cancer and Chronic Pancreatitis: Rationale and Methodology for the DETECT Study From the Consortium for the Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer. 2018

Hart, Phil A / Andersen, Dana K / Mather, Kieren J / Castonguay, Alicia C / Bajaj, Mandeep / Bellin, Melena D / Bradley, David / Contreras, Noemy / Habtezion, Aida / Korc, Murray / Kudva, Yogish / Petrov, Maxim S / Whitcomb, David C / Yadav, Dhiraj / Yuan, Ying / Rinaudo, Jo Ann S / Srivastava, Sudhir / Serrano, Jose / Goodarzi, Mark O / Anonymous3710965. ·Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD. · Division of Endocrinology and Metabolism, Indiana University School of Medicine, Indianapolis, IN. · Section of Endocrinology, Diabetes and Metabolism, Baylor College of Medicine, Houston, TX. · Departments of Pediatrics and Surgery, University of Minnesota Medical School, Minneapolis, MN. · Diabetes and Metabolism Research Center, Division of Endocrinology, Diabetes and Metabolism, The Ohio State University Wexner Medical Center, Columbus, OH. · Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX. · Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA. · Departments of Medicine, and Biochemistry and Molecular Biology, Indiana University School of Medicine, the Melvin and Bren Simon Cancer Center, and the Pancreatic Cancer Signature Center, Indianapolis, IN. · Division of Endocrinology, Mayo Clinic College of Medicine, Rochester, MN. · Department of Surgery, University of Auckland, Auckland, New Zealand. · Departments of Medicine, Cell Biology and Molecular Physiology, and Human Genetics, University of Pittsburgh, and UPMC. · Division of Gastroenterology and Hepatology, University of Pittsburgh Medical Center, Pittsburgh, PA. · Cancer Biomarker Research Group, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Rockville, MD. · Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA. ·Pancreas · Pubmed #30325863.

ABSTRACT: Pancreatogenic diabetes mellitus is most commonly the result of chronic pancreatitis but can also occur secondary to pancreatic cancer. The early identification of pancreatogenic diabetes and distinction from the more prevalent type 2 diabetes are clinically significant; however, currently, there is no validated method to differentiate these diabetes subtypes. We describe a study, "Evaluation of a Mixed Meal Test for Diagnosis and Characterization of PancrEaTogEniC DiabeTes Secondary to Pancreatic Cancer and Chronic Pancreatitis: the DETECT study," that seeks to address this knowledge gap. The DETECT study is a multicenter study that will examine differences in hormone and glucose excursions after a mixed meal test. The study will also create a biorepository that will be used to evaluate novel diagnostic biomarkers for differentiating these diabetes subtypes.

15 Article PROspective Evaluation of Chronic Pancreatitis for EpidEmiologic and Translational StuDies: Rationale and Study Design for PROCEED From the Consortium for the Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer. 2018

Yadav, Dhiraj / Park, Walter G / Fogel, Evan L / Li, Liang / Chari, Suresh T / Feng, Ziding / Fisher, William E / Forsmark, Christopher E / Jeon, Christie Y / Habtezion, Aida / Hart, Phil A / Hughes, Steven J / Othman, Mohamed O / Rinaudo, Jo Ann S / Pandol, Stephen J / Tirkes, Temel / Serrano, Jose / Srivastava, Sudhir / Van Den Eeden, Stephen K / Whitcomb, David C / Topazian, Mark / Conwell, Darwin L / Anonymous3700965. ·Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine, Palo Alto, CA. · Digestive and Liver Disorders, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN. · Department of Biostatistics, University of Texas MD Anderson Cancer Center, Houston, TX. · Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN. · Biostatistics Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA. · Division of General Surgery, Baylor College of Medicine, Houston, TX. · Division of Gastroenterology, Hepatology, and Nutrition, University of Florida, Gainesville, FL. · Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA. · Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, OH. · Department of Surgery, University of Florida, Gainesville, FL. · Gastroenterology and Hepatology Section, Baylor College of Medicine, Houston, TX. · Cancer Biomarker Research Group, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Rockville, MD. · Division of Digestive and Liver Diseases, Cedars-Sinai Medical Center, Los Angeles, CA. · Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN. · Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD. · Division of Research, Kaiser Permanente Northern California, Oakland, CA. ·Pancreas · Pubmed #30325862.

ABSTRACT: Prospective Evaluation of Chronic Pancreatitis for Epidemiologic and Translational Studies (PROCEED) is the first prospective, observational cohort study of chronic pancreatitis (CP) in the United States. The primary goals of PROCEED are to define disease progression, test the predictive capability of candidate biomarkers, and develop a platform to conduct translational and mechanistic studies in CP. Using objective and consensus-driven criteria, PROCEED will enroll adults at different stages of CP-controls, suspected CP, and definite CP. In addition to collecting detailed information using structured case report forms and protocol-mandated evaluations at baseline and during follow-up, PROCEED will establish a linked biorepository of blood, urine, saliva, stool, pancreatic fluid, and pancreatic tissue. Enrollment for PROCEED began in June 2017. As of July 1, 2018, nine clinical centers of the Consortium for the Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer are enrolling, and 350 subjects have completed baseline evaluation. In conclusion, PROCEED will provide the most accurate and reliable estimates to date on progression of CP. The established cohort and biorepository will facilitate numerous analyses, leading to new strategies for diagnosis, methods to monitor disease progression, and treatment of CP.

16 Article Standard Operating Procedures for Biospecimen Collection, Processing, and Storage: From the Consortium for the Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer. 2018

Fisher, William E / Cruz-Monserrate, Zobeida / McElhany, Amy L / Lesinski, Gregory B / Hart, Phil A / Ghosh, Ria / Van Buren, George / Fishman, Douglas S / Rinaudo, Jo Ann S / Serrano, Jose / Srivastava, Sudhir / Mace, Thomas / Topazian, Mark / Feng, Ziding / Yadav, Dhiraj / Pandol, Stephen J / Hughes, Steven J / Liu, Robert Y / Lu, Emily / Orr, Robert / Whitcomb, David C / Abouhamze, Amer S / Steen, Hanno / Sellers, Zachary M / Troendle, David M / Uc, Aliye / Lowe, Mark E / Conwell, Darwin L / Anonymous3680965. ·Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, and Comprehensive Cancer Center, The Ohio State University Wexner Medical Center, Columbus, OH. · Winship Cancer Institute, Department of Hematology and Medical Oncology, Emory University, Atlanta, GA. · Department of Biostatistics, The University of Texas MD Anderson Cancer Center. · Department of Pediatrics, Baylor College of Medicine, Houston, TX. · Cancer Biomarkers Research Group, Division of Cancer Prevention, National Cancer Institute, Rockville. · Division of Digestive Diseases and Nutrition, National Institutes of Diabetes and Digestive and Kidney Diseases, Bethesda, MD. · Department of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN. · Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Pittsburgh, Pittsburgh, PA. · Division of Digestive and Liver Diseases, Cedars-Sinai Medical Center, Los Angeles, CA. · Department of Surgery, University of Florida College of Medicine, Gainesville, FL. · Clinical Research Support Center, The University of Texas MD Anderson Cancer Center, Houston, TX. · Indiana Clinical and Translational Sciences Institute, Specimen Storage Facility, Indianapolis, IN. · Clinical and Translational Sciences, University of Florida, Gainesville, FL. · Departments of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, MA. · Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Lucile Packard Children's Hospital and Stanford University School of Medicine, Stanford, CA. · Department of Pediatrics, University of Texas Southwestern Medical School, Dallas, TX. · Stead Family Department of Pediatrics, University of Iowa, Stead Family Children's Hospital, Iowa City, IA. · Department of Pediatrics, Washington University School of Medicine, St Louis, MO. ·Pancreas · Pubmed #30325860.

ABSTRACT: High-quality and well-annotated biorepositories are needed to better understand the pathophysiology and biologic mechanisms of chronic pancreatitis (CP) and its consequences. We report a methodology for the development of a robust standard operating procedure (SOP) for a biorepository based on the experience of the clinical centers within the consortium to study Chronic Pancreatitis, Diabetes and Pancreas Cancer Clinical Centers (CPDPC), supported by the National Cancer Institute and the National Institute for Diabetes and Digestive and Kidney Diseases as a unique multidisciplinary model to study CP, diabetes, and pancreatic cancer in both children and adults. Standard operating procedures from the CPDPC centers were evaluated and consolidated. The literature was reviewed for standard biorepository operating procedures that facilitated downstream molecular analysis. The existing literature on biobanking practices was harmonized with the SOPs from the clinical centers to produce a biorepository for pancreatic research. This article reports the methods and basic principles behind the creation of SOPs to develop a biorepository for the CPDPC. These will serve as a guide for investigators developing biorepositories in pancreas research. Rigorous and meticulous adherence to standardized biospecimen collection will facilitate investigations to better understand the pathophysiology and biologic mechanisms of CP, diabetes, and pancreatic cancer.

17 Article Consortium for the Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer: From Concept to Reality. 2018

Serrano, Jose / Andersen, Dana K / Forsmark, Christopher E / Pandol, Stephen J / Feng, Ziding / Srivastava, Sudhir / Rinaudo, Jo Ann S / Anonymous3670965. ·Division of Gastroenterology, Department of Medicine, University of Florida Health Sciences Center, Gainesville, FL. · Division of Gastroenterology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA. · Department of Biostatistics, University of Texas MD Anderson Cancer Center, Houston, TX. · Cancer Biomarker Research Group, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Rockville, MD. ·Pancreas · Pubmed #30325859.

ABSTRACT: Research progress in diseases of the exocrine pancreas [chronic pancreatitis (CP), pancreatogenic diabetes mellitus, and pancreatic cancer] has been hampered by the disorders' heterogeneity, the limitations of previous small cross-sectional studies, the inability to safely obtain pancreatic tissue for study, and the lack of structured epidemiology tools, genetic testing, and biomarker development. Mechanism-based research of these diseases has suffered from the lack of systematically collected clinical measures in longitudinal cohort studies linked with biospecimens. Given the increasing incidence and prevalence of CP and its association to the development of pancreatic cancer, its complications, high mortality rate, and associated health care cost, the National Institute for Diabetes and Digestive and Kidney Diseases and the National Cancer Institute funded the Consortium for the Study of Chronic Pancreatitis, Diabetes and Pancreatic Cancer to identify research gaps and foster multidisciplinary collaborations to better diagnose, characterize, and manage CP and its sequelae. The CPDPC structure, governance, and research objectives are described in this article. Studies undertaken by the CPDPC are described in other articles in this journal's issue.

18 Article Pharmacokinetic evaluation of the PNC disassembler metarrestin in wild-type and Pdx1-Cre;LSL-Kras 2018

Vilimas, Tomas / Wang, Amy Q / Patnaik, Samarjit / Hughes, Emma A / Singleton, Marc D / Knotts, Zachary / Li, Dandan / Frankowski, Kevin / Schlomer, Jerome J / Guerin, Theresa M / Springer, Stephanie / Drennan, Catherine / Dextras, Christopher / Wang, Chen / Gilbert, Debra / Southall, Noel / Ferrer, Marc / Huang, Sui / Kozlov, Serguei / Marugan, Juan / Xu, Xin / Rudloff, Udo. ·Molecular Characterization Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc., Frederick, MD, 21702, USA. · Therapeutics for Rare and Neglected Diseases (TRND) Program, National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Rockville, MD, 20850, USA. · Division of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Rockville, MD, 20850, USA. · Department of Bioengineering and Therapeutic Sciences, University of California San Francisco, San Francisco, CA, 94158, USA. · Biophysics Graduate Group, University of California Berkeley, Berkeley, CA, 94720, USA. · Rare Tumor Initiative (RTI), Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, Hatfield Center, 10 Center Drive, 9000 Rockville Pike, Bethesda, MD, 20892, USA. · Department of Medicinal Chemistry and Specialized Chemistry Center, University of Kansas, Lawrence, KS, USA. · Center for Advanced Preclinical Research, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc., Frederick, MD, 21702, USA. · Department of Cell and Molecular Biology, Northwestern University, Chicago, IL, 60611, USA. · Division of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Rockville, MD, 20850, USA. maruganj@mail.nih.gov. · NIH Chemical Genomics Center, National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Bldg B, Rockville, MD, 20850, USA. maruganj@mail.nih.gov. · Therapeutics for Rare and Neglected Diseases (TRND) Program, National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Rockville, MD, 20850, USA. xin.xu3@nih.gov. · Rare Tumor Initiative (RTI), Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, Hatfield Center, 10 Center Drive, 9000 Rockville Pike, Bethesda, MD, 20892, USA. rudloffu@mail.nih.gov. ·Cancer Chemother Pharmacol · Pubmed #30306263.

ABSTRACT: PURPOSE: Metarrestin is a first-in-class small molecule clinical candidate capable of disrupting the perinucleolar compartment, a subnuclear structure unique to metastatic cancer cells. This study aims to define the pharmacokinetic (PK) profile of metarrestin and the pharmacokinetic/pharmacodynamic relationship of metarrestin-regulated markers. METHODS: PK studies included the administration of single or multiple dose of metarrestin at 3, 10, or 25 mg/kg via intravenous (IV) injection, gavage (PO) or with chow to wild-type C57BL/6 mice and KPC mice bearing autochthonous pancreatic tumors. Metarrestin concentrations were analyzed by UPLC-MS/MS. Pharmacodynamic assays included mRNA expression profiling by RNA-seq and qRT-PCR for KPC mice. RESULTS: Metarrestin had a moderate plasma clearance of 48 mL/min/kg and a large volume of distribution of 17 L/kg at 3 mg/kg IV in C57BL/6 mice. The oral bioavailability after single-dose (SD) treatment was > 80%. In KPC mice treated with SD 25 mg/kg PO, plasma AUC CONCLUSIONS: Metarrestin is an effective therapeutic candidate with a favorable PK profile achieving excellent intratumor tissue levels in a disease with known poor drug delivery.

19 Article Prospective metabolomics study identifies potential novel blood metabolites associated with pancreatic cancer risk. 2018

Shu, Xiang / Zheng, Wei / Yu, Danxia / Li, Hong-Lan / Lan, Qing / Yang, Gong / Cai, Hui / Ma, Xiao / Rothman, Nathaniel / Gao, Yu-Tang / Jia, Wei / Xiang, Yong-Bing / Shu, Xiao-Ou. ·Division of Epidemiology, Department of Medicine, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN. · State Key Laboratory of Oncogene and Related Genes & Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. · Division of Cancer Epidemiology and Genetics, Occupational and Environmental Epidemiology Branch, National Cancer Institute, Rockville, MD. · Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI. · Center for Translational Medicine, and Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China. ·Int J Cancer · Pubmed #29717485.

ABSTRACT: Using a metabolomics approach, we systematically searched for circulating metabolite biomarkers for pancreatic cancer risk in a case-control study nested within two prospective Shanghai cohorts. Included in our study were 226 incident pancreatic cancer cases and their individually-matched controls. Untargeted mass spectrometry platforms were used to measure metabolites in blood samples collected prior to cancer diagnosis. Conditional logistic regression was performed to assess the associations of metabolites with pancreatic cancer risk. We identified 10 metabolites associated with pancreatic cancer, after accounting for multiple comparisons (the Benjamini-Hochberg false discovery rate <0.05). The majority of the identified metabolites were glycerophospholipids (ORs per SD increase: 0.44-2.32; p values: 7.2 × 10

20 Article Association of Cigarette, Cigar, and Pipe Use With Mortality Risk in the US Population. 2018

Christensen, Carol H / Rostron, Brian / Cosgrove, Candace / Altekruse, Sean F / Hartman, Anne M / Gibson, James T / Apelberg, Benjamin / Inoue-Choi, Maki / Freedman, Neal D. ·Office of Science, Center for Tobacco Products, Food and Drug Administration, Silver Spring, Maryland. · United States Census Bureau, Suitland, Maryland. · National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. · Tobacco Control Research Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. · Information Management Services, Inc. · Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland. ·JAMA Intern Med · Pubmed #29459935.

ABSTRACT: Importance: Tobacco products have changed in recent years. Contemporary mortality risk estimates of combustible tobacco product use are needed. Objective: To investigate the mortality risks associated with current and former use of cigars, pipes, and cigarettes. Design, Setting, and Participants: The National Longitudinal Mortality Study is a longitudinal population-based, nationally representative health survey with mortality follow-up that includes demographic and other information from the Current Population Survey, tobacco product use information from the Tobacco Use Supplement, and mortality data from the National Death Index. In this study, participants provided tobacco use information at baseline in surveys starting from 1985 and were followed for mortality through the end of 2011. The study includes 357 420 participants who reported exclusively using cigar, pipes, or cigarettes or reported never using any type of tobacco product. Exposures: Current or former exclusive use of any cigar (little cigar, cigarillos, large cigar), traditional pipe, or cigarette and never tobacco use. Information on current daily and nondaily use was also collected. Estimates adjusted for age, sex, race/ethnicity, education, and survey year. Main Outcomes and Measures: All-cause and cause-specific mortality as identified as the primary cause of death from death certificate information. Results: Of the 357 420 persons included in the analysis, the majority of current and former cigar and pipe smokers were male (79.3%-98.0%), and smokers were more evenly divided by sex (46% of current daily smokers were male). There were 51 150 recorded deaths during follow-up. Exclusive current cigarette smokers (hazard ratio [HR], 1.98; 95% CI, 1.93-2.02) and exclusive current cigar smokers (HR, 1.20; 95% CI, 1.03-1.38) had higher all-cause mortality risks than never tobacco users. Exclusive current cigarette smokers (HR, 4.06; 95% CI, 3.84-4.29), exclusive current cigar smokers (HR, 1.61; 95% CI, 1.11-2.32), and exclusive current pipe smokers (HR, 1.58; 95% CI, 1.05-2.38) had an elevated risk of dying from a tobacco-related cancer (including bladder, esophagus, larynx, lung, oral cavity, and pancreas). Among current nondaily cigarette users, statistically significant associations were observed with deaths from lung cancer (HR, 6.24; 95% CI, 5.17-7.54), oral cancer (HR, 4.62; 95% CI, 1.84-11.58), circulatory death (HR, 1.43; 95% CI, 1.30-1.57), cardiovascular death (HR, 1.24; 95% CI, 1.11-1.39), cerebrovascular death (stroke) (HR, 1.39; 95% CI, 1.12-1.74), and chronic obstructive pulmonary disease (HR, 7.66; 95% CI, 6.09-9.64) as well as for daily smokers. Conclusions and Relevance: This study provides further evidence that exclusive use of cigar, pipes, and cigarettes each confers significant mortality risks.

21 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

22 Article Is the Women's Health Initiative (WHI) Dietary Modification Associated With a Reduced Risk of Pancreatic Cancer? 2018

Stolzenberg-Solomon, Rachael Z / Katki, Hormuzd A. ·Metabolic Epidemiology Branch and Biostatics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville MD. ·J Natl Cancer Inst · Pubmed #28922785.

ABSTRACT: -- No abstract --

23 Article Childhood body mass index and risk of adult pancreatic cancer. 2017

Nogueira, Leticia / Stolzenberg-Solomon, Rachael / Gamborg, Michael / Sørensen, Thorkild I A / Baker, Jennifer L. ·Texas Cancer Registry, Texas Department of State Health Services, Austin TX. · Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville MD. · Department of Clinical Epidemiology, Bispebjerg and Frederiksberg Hospital, Copenhagen University Hospital, Copenhagen, Denmark. · Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. ·Curr Dev Nutr · Pubmed #29388617.

ABSTRACT: Background: Excess weight in adulthood is one of the few modifiable risk factors for pancreatic cancer, and height has associations as well. This leads to question whether body weight and height in childhood are associated with adult pancreatic cancer. Objective: To examine if childhood body mass index (BMI; kg/m Methods: We linked 293,208 children born from 1930-1982 in the Copenhagen School Health Records Register who had measured values of weights and heights at ages 7-13 years with the Danish Cancer Registry to identify incident pancreatic cancer cases from 1968-2012. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated using Cox proportional hazard regressions. Results: During 8,207,015 person-years of follow-up, 1,268 pancreatic cancer cases were diagnosed. Childhood BMI z-scores at ages 7-13 years were positively and significantly associated with pancreatic cancer in men and women up to age 70 years; beyond age 70 the associations diminished. The HRs of pancreatic cancer were 1.13 (95% CI: 1.05-1.21) and 1.18 (95% CI: 1.09-1.27) per BMI z-score at ages 7 and 13 years, respectively. A BMI ≥1.5 z-score at ages 7, 10 and 13 years was positively and significantly associated with pancreatic cancer; however, the effect did not differ from having a BMI z-score ≥1.5 at only one of these ages. Positive, albeit non-statistically significant, associations were identified with height. Conclusions: BMI at all ages from 7-13 years is positively and linearly associated with adult pancreatic cancer; the higher the BMI, the higher the risk. Excess childhood BMI may be indicative of processes initiated early in life that lead to this cancer. Prevention of childhood adiposity may decrease the burden of pancreatic cancer in adults.

24 Article Prediagnosis Circulating Insulin-Like Growth Factors and Pancreatic Cancer Survival. 2017

Toriola, Adetunji T / Ziegler, Mark / Li, Yize / Pollak, Michael / Stolzenberg-Solomon, Rachael. ·Department of Surgery, Division of Public Health Sciences, and Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO, USA. a.toriola@wustl.edu. · Department of Surgery, Division of Public Health Sciences, and Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO, USA. · Department of Oncology, McGill University, Montreal, Canada. · Branch of Nutritional Epidemiology, Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Rockville, MD, USA. ·Ann Surg Oncol · Pubmed #28681154.

ABSTRACT: BACKGROUND: Prediagnosis obesity and diabetes are associated with survival from pancreatic cancer, but the underlying mechanisms have not been characterized. Because both are associated with dysregulation in circulating insulin-like growth factor (IGF) levels, we evaluated the associations of prediagnosis IGF levels (IGF-I, IGF-II) and IGF binding protein 3 (IGFBP-3) with pancreatic cancer survival. METHODS: Participants were subjects enrolled in the intervention arm of the PLCO Cancer Screening Trial who developed exocrine pancreatic cancer during follow-up (N = 178, 116 men and 67 women). Participants provided blood samples at enrollment, before cancer diagnosis. Cox proportional hazards regression model, adjusted for confounders was used to investigate associations of IGF biomarkers with pancreatic cancer survival. Because of the well-documented, gender-specific differences in circulating IGF biomarkers, and differential associations of IGF biomarkers with mortality, we evaluated associations separately among males and females. RESULTS: Median survival was 172 days. Higher IGF-II and IGFBP-3 levels were associated with pancreatic cancer survival among males but not among females. The hazard ratios (HR) of death among men in the highest tertiles of IGF-II and IGFBP-3 compared with men in the lowest tertiles were 0.40 (95% confidence interval (CI) 0.23-0.71, p < 0.01) and 0.59 (95% CI 0.35-0.97, p = 0.10), respectively. There were no statistically significant associations between IGF-I concentrations, IGF-I/IGFBP-3, and pancreatic cancer survival. CONCLUSIONS: Higher prediagnosis circulating IGF-II and IGFBP-3 levels are associated with better pancreatic cancer survival among men but not women. A greater understanding of how IGF signaling is related to pancreatic cancer survival could have utility in improving pancreatic cancer prognosis.

25 Article A Plasma Biomarker Panel to Identify Surgically Resectable Early-Stage Pancreatic Cancer. 2017

Balasenthil, Seetharaman / Huang, Ying / Liu, Suyu / Marsh, Tracey / Chen, Jinyun / Stass, Sanford A / KuKuruga, Debra / Brand, Randall / Chen, Nanyue / Frazier, Marsha L / Jack Lee, J / Srivastava, Sudhir / Sen, Subrata / McNeill Killary, Ann. ·Department of Translational Molecular Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA. · Fred Hutchison Cancer Research Center, Seattle, WA, USA. · Department of Biostatistics, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA. · Department of Epidemiology, University of Maryland Medical Center , Baltimore, MD, USA. · University of Maryland Medical Center , Baltimore, MD, USA. · University of Pittsburgh Medical Center, Pittsburgh, PA, USA. · National Cancer Institute, Rockville, MD, USA. ·J Natl Cancer Inst · Pubmed #28376184.

ABSTRACT: Background: Blood-based biomarkers for early detection of pancreatic ductal adenocarcinoma (PDAC) are urgently needed. Current biomarkers lack high sensitivity and specificity for population screening. The gold-standard biomarker, CA 19-9, also fails to demonstrate the predictive value necessary for early detection. Methods: To validate a functional genomics-based plasma migration signature biomarker panel, plasma tissue factor pathway inhibitor (TFPI), tenascin C (TNC-FN III-C), and CA 19-9 levels were measured by enzyme-linked immunosorbent assays in three early-stage PDAC plasma cohorts, including two independent blinded validation cohorts containing a total of 43 stage I, 163 stage II, 86 chronic pancreatitis, 31 acute biliary obstruction, and 108 controls. Logistic regression models developed classification rules combining TFPI and/or TNC-FN III-C with CA 19-9 for patient cases and control subjects, with or without adjustment for age and diabetes status. Model classification performance was evaluated and analyses repeated among subpopulations without diabetes and pancreatitis history. Two-sided P values were calculated using bootstrap method. Results: The TFPI/TNC-FN III-C/CA 19-9 panel improved CA 19-9 performance in all early-stage cohorts, including discriminating stage IA/IB/IIA, stage IIB, and all early-stage cancer from healthy controls. Statistical significance was reached for a number of subcohorts, including for all early-stage cancer vs healthy controls (cohort 1 AUC = 0.92, 95% CI = 0.86 to 0.96, P  = .04; cohort 3 AUC = 0.83, 95% CI = 0.76 to 0.89, P  = .045). Among subcohorts without diabetes and pancreatitis history, the panel approaches potential clinical utility for early detection to discriminate early-stage PDAC from healthy controls including an area under the curve (AUC) of 0.87 (95% CI = 0.77 to 0.95) for stage I/IIA, an AUC of 0.93 (95% CI = 0.87 to 0.98) for stage IIB, and a statistically significant AUC of 0.89 (95% CI = 0.82 to 0.95) for all early-stage cancer ( P  = .03). Conclusions: TFPI/TNC-FN III-C migration signature adds statistically significantly to CA 19-9's predictive power to detect early-stage PDAC and may have clinical utility for early detection of surgically resectable PDAC, as well as for enhanced survival from this routinely lethal cancer.

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