Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Pancreatic Neoplasms: HELP
Articles by Amy L. McElhany
Based on 7 articles published since 2010
(Why 7 articles?)
||||

Between 2010 and 2020, Amy McElhany wrote the following 7 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Nutritional and Metabolic Derangements in Pancreatic Cancer and Pancreatic Resection. 2017

Gilliland, Taylor M / Villafane-Ferriol, Nicole / Shah, Kevin P / Shah, Rohan M / Tran Cao, Hop S / Massarweh, Nader N / Silberfein, Eric J / Choi, Eugene A / Hsu, Cary / McElhany, Amy L / Barakat, Omar / Fisher, William / Van Buren, George. ·The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. Taylor.Gilliland@bcm.edu. · The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. Nicole.Villafane@bcm.edu. · The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. Kevin.Shah@bcm.edu. · The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. Rohan.Shah@bcm.edu. · The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. Hop.TranCao@bcm.edu. · The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. Nader.Massarweh@bcm.edu. · The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. ejs@bcm.edu. · The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. Eugene.Choi@bcm.edu. · The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. Cary.Hsu@bcm.edu. · The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. Amy.McElhany@bcm.edu. · The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. Omar.Barakat@bcm.edu. · The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. wfisher@bcm.edu. · The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. George.vanburen@bcm.edu. ·Nutrients · Pubmed #28272344.

ABSTRACT: Pancreatic cancer is an aggressive malignancy with a poor prognosis. The disease and its treatment can cause significant nutritional impairments that often adversely impact patient quality of life (QOL). The pancreas has both exocrine and endocrine functions and, in the setting of cancer, both systems may be affected. Pancreatic exocrine insufficiency (PEI) manifests as weight loss and steatorrhea, while endocrine insufficiency may result in diabetes mellitus. Surgical resection, a central component of pancreatic cancer treatment, may induce or exacerbate these dysfunctions. Nutritional and metabolic dysfunctions in patients with pancreatic cancer lack characterization, and few guidelines exist for nutritional support in patients after surgical resection. We reviewed publications from the past two decades (1995-2016) addressing the nutritional and metabolic status of patients with pancreatic cancer, grouping them into status at the time of diagnosis, status at the time of resection, and status of nutritional support throughout the diagnosis and treatment of pancreatic cancer. Here, we summarize the results of these investigations and evaluate the effectiveness of various types of nutritional support in patients after pancreatectomy for pancreatic adenocarcinoma (PDAC). We outline the following conservative perioperative strategies to optimize patient outcomes and guide the care of these patients: (1) patients with albumin < 2.5 mg/dL or weight loss > 10% should postpone surgery and begin aggressive nutrition supplementation; (2) patients with albumin < 3 mg/dL or weight loss between 5% and 10% should have nutrition supplementation prior to surgery; (3) enteral nutrition (EN) should be preferred as a nutritional intervention over total parenteral nutrition (TPN) postoperatively; and, (4) a multidisciplinary approach should be used to allow for early detection of symptoms of endocrine and exocrine pancreatic insufficiency alongside implementation of appropriate treatment to improve the patient's quality of life.

2 Article SRC-3 inhibition blocks tumor growth of pancreatic ductal adenocarcinoma. 2019

Song, Xianzhou / Chen, Hui / Zhang, Chengwei / Yu, Yang / Chen, Zhongyuan / Liang, Han / Van Buren, George / McElhany, Amy L / Fisher, William E / Lonard, David M / O'Malley, Bert W / Wang, Jin. ·Department of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, TX, 77030, USA. · Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, 77030, USA. · Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA; Department of Statistics, Rice University, Houston, TX, 77030, USA. · Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA; Department of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA. · Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX, 77030, USA. · Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, 77030, USA. Electronic address: dlonard@bcm.edu. · Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, 77030, USA. Electronic address: berto@bcm.edu. · Department of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, TX, 77030, USA; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, 77030, USA. Electronic address: wangj@bcm.edu. ·Cancer Lett · Pubmed #30423406.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is a highly malignant and lethal disease with few treatment options. Steroid receptor coactivator-3 (SRC-3, also known as NCOA3, AIB1, pCIP, ACTR, RAC3, TRAM1) sits at the nexus of many growth signaling pathways and has been pursued as a therapeutic target for breast, prostate and lung cancers. In this study, we find that SRC-3 is overexpressed in PDAC and inversely correlates with patient overall survival. Knockdown of SRC-3 reduces pancreatic cancer cell proliferation, migration and invasion in vitro. Additionally, inhibition of SRC-3 using either shRNA or a small molecule inhibitor can significantly inhibit tumor growth in orthotopic pancreatic cancer mouse models. Collectively, this study establishes SRC-3 as a promising therapeutic target for pancreatic cancer treatment.

3 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.

4 Article Venous thrombosis following pancreaticoduodenectomy with venous resection. 2018

Mohammed, Somala / Mendez-Reyes, Jose E / McElhany, Amy / Gonzales-Luna, Daniel / Van Buren, George / Bland, Daniel S / Villafane-Ferriol, Nicole / Pierzynski, Jeanne A / West, Charles A / Silberfein, Eric J / Fisher, William E. ·Baylor College of Medicine, The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, Houston, Texas. · Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas. · Baylor College of Medicine, The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, Houston, Texas. Electronic address: wfisher@bcm.edu. ·J Surg Res · Pubmed #29907222.

ABSTRACT: BACKGROUND: Addition of en bloc segmental venous reconstruction (VR) to pancreaticoduodenectomy (PD) for venous involvement of pancreatic tumors increases the complexity of the operation and may increase complications. The long-term mesenteric venous patency rate and oncologic outcome has not been well defined. METHODS: Our prospective database was reviewed to assess 90-day postoperative outcomes for patients who underwent PD or PD + VR (September 2004-June 2016). Two independent observers reviewed CT scans to determine long-term vein patency. In patients with pancreatic ductal adenocarcinoma, the impact of VR on 5-year overall survival was assessed using multivariate Cox proportional hazards regression. Student's t-test was used to evaluate continuous variables and the chi-square test for categorical variables. RESULTS: Three hundred ninety-three patients underwent PD (51 PD + VR). Patients undergoing PD + VR had longer operations (561 ± 119 versus 433 ± 89 min, P < 0.00001) and greater blood loss (768 ± 812 versus 327 ± 423 cc, P < 0.00001). There was no difference in 90-day mortality, overall postoperative complication rates, complication severity grades, reoperation, readmission, or length of stay. 26.7% experienced venous thrombosis. Most thromboses occurred in the first year after surgery, but we also observed late thrombosis in 1 patient after 89-month follow-up. Among 135 patients with pancreatic ductal adenocarcinoma, survival was significantly longer in the PD-alone group (31.3 months [95% confidence interval: 22.9-40.0] versus 17.0 [95% confidence interval: 13.0-19.1], p CONCLUSIONS: PD + VR does not increase short-term morbidity, but venous thrombosis is frequent and can occur long after surgery. Survival is inferior when VR is required especially in the absence of neoadjuvant chemotherapy.

5 Article Pancreatic endometrial cyst mimics mucinous cystic neoplasm of the pancreas. 2017

Mederos, Michael A / Villafañe, Nicole / Dhingra, Sadhna / Farinas, Carlos / McElhany, Amy / Fisher, William E / Van Buren Ii, George. ·Michael A Mederos, Nicole Villafañe, Amy McElhany, William E Fisher, George Van Buren II, Department of General Surgery, Baylor College of Medicine, Houston, TX 77030, United States. ·World J Gastroenterol · Pubmed #28246486.

ABSTRACT: Pancreatic cysts include a variety of benign, premalignant, and malignant lesions. Endometrial cysts in the pancreas are exceedingly rare lesions that are difficult to diagnose pre-operatively. This report describes the findings in a 43-year-old patient with a recent episode of acute pancreatitis who presented with a large cyst in the tail of the pancreas. Imaging demonstrated a loculated pancreatic cyst, and cyst fluid aspiration revealed an elevated amylase and carcinoembryonic antigen. The patient experienced an interval worsening of abdominal pain, fatigue, diarrhea, and a 15-pound weight loss 3 mo after the initial episode of pancreatitis. With concern for a possible pre-malignant lesion, the patient underwent a laparoscopic distal pancreatectomy with splenectomy, which revealed a 16 cm × 12 cm × 4 cm lesion. Final histopathology was consistent with an intra-pancreatic endometrial cyst. Here we discuss the overlapping imaging and laboratory features of pancreatic endometrial cysts and mucinous cystic neoplasms of the pancreas.

6 Article Ampullary Cancers Harbor ELF3 Tumor Suppressor Gene Mutations and Exhibit Frequent WNT Dysregulation. 2016

Gingras, Marie-Claude / Covington, Kyle R / Chang, David K / Donehower, Lawrence A / Gill, Anthony J / Ittmann, Michael M / Creighton, Chad J / Johns, Amber L / Shinbrot, Eve / Dewal, Ninad / Fisher, William E / Anonymous400856 / Pilarsky, Christian / Grützmann, Robert / Overman, Michael J / Jamieson, Nigel B / Van Buren, George / Drummond, Jennifer / Walker, Kimberly / Hampton, Oliver A / Xi, Liu / Muzny, Donna M / Doddapaneni, Harsha / Lee, Sandra L / Bellair, Michelle / Hu, Jianhong / Han, Yi / Dinh, Huyen H / Dahdouli, Mike / Samra, Jaswinder S / Bailey, Peter / Waddell, Nicola / Pearson, John V / Harliwong, Ivon / Wang, Huamin / Aust, Daniela / Oien, Karin A / Hruban, Ralph H / Hodges, Sally E / McElhany, Amy / Saengboonmee, Charupong / Duthie, Fraser R / Grimmond, Sean M / Biankin, Andrew V / Wheeler, David A / Gibbs, Richard A. ·Department of Molecular and Human Genetics, Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX 77030, USA; Michael DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX 77030, USA; Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: mgingras@bcm.edu. · Department of Molecular and Human Genetics, Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX 77030, USA. · Wolfson Wohl Cancer Research Centre, Institute for Cancer Sciences, University of Glasgow, Garscube Estate, Bearsden, Glasgow G61 1BD, UK; West of Scotland Pancreatic Unit, Glasgow Royal Infirmary, Glasgow G31 2ER, UK; The Kinghorn Cancer Centre and the Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, Sydney, NSW 2010, Australia; South Western Sydney Clinical School, Faculty of Medicine, University of New South Wales, Liverpool, NSW 2170, Australia. · Department of Molecular and Human Genetics, Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX 77030, USA; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030, USA. · The Kinghorn Cancer Centre and the Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, Sydney, NSW 2010, Australia; Department of Anatomical Pathology, Royal North Shore Hospital, St Leonards, Sydney, NSW 2065, Australia; Sydney Medical School, University of Sydney, Sydney, NSW 2006, Australia. · Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA; Department of Pathology and Immunology, Baylor College of Medicine, Houston, TX 77030, USA; Michael E. DeBakey Department of Veterans Affairs Medical Center, Houston, TX 77030, USA. · Department of Molecular and Human Genetics, Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX 77030, USA; Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. · The Kinghorn Cancer Centre and the Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, Sydney, NSW 2010, Australia. · Michael DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX 77030, USA; Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA; The Elkins Pancreas Center at Baylor College of Medicine, Houston, TX 77030, USA. · Department of Surgery, TU Dresden, 01307 Dresden, Germany. · Department of Surgery, Universitätsklinikum Erlangen, 91054 Erlangen, Germany. · Department of Gastrointestinal Medical Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. · Wolfson Wohl Cancer Research Centre, Institute for Cancer Sciences, University of Glasgow, Garscube Estate, Bearsden, Glasgow G61 1BD, UK; West of Scotland Pancreatic Unit, Glasgow Royal Infirmary, Glasgow G31 2ER, UK; Academic Unit of Surgery, Institute of Cancer Sciences, Glasgow Royal Infirmary, Level 2, New Lister Building, University of Glasgow, Glasgow G31 2ER, UK. · Sydney Medical School, University of Sydney, Sydney, NSW 2006, Australia; Department of Surgery, Royal North Shore Hospital, St Leonards, Sydney, NSW 2065, Australia. · Wolfson Wohl Cancer Research Centre, Institute for Cancer Sciences, University of Glasgow, Garscube Estate, Bearsden, Glasgow G61 1BD, UK. · Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, QLD 4072, Australia; QIMR Berghofer Medical Research Institute, Herston, Brisbane, QLD 4006, Australia. · Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, QLD 4072, Australia. · Department of Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. · Department of Pathology, TU Dresden, 01307 Dresden, Germany. · Wolfson Wohl Cancer Research Centre, Institute for Cancer Sciences, University of Glasgow, Garscube Estate, Bearsden, Glasgow G61 1BD, UK; Department of Pathology, Southern General Hospital, Greater Glasgow and Clyde NHS, Glasgow G51 4TF, UK. · Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, the Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. · Michael DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX 77030, USA; The Elkins Pancreas Center at Baylor College of Medicine, Houston, TX 77030, USA. · Department of Molecular and Human Genetics, Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX 77030, USA; Department of Biochemistry and Liver Fluke and Cholangiocarcinoma Research Center, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand. · Wolfson Wohl Cancer Research Centre, Institute for Cancer Sciences, University of Glasgow, Garscube Estate, Bearsden, Glasgow G61 1BD, UK; Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, QLD 4072, Australia. · Department of Molecular and Human Genetics, Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX 77030, USA; Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: wheeler@bcm.edu. ·Cell Rep · Pubmed #26804919.

ABSTRACT: The ampulla of Vater is a complex cellular environment from which adenocarcinomas arise to form a group of histopathologically heterogenous tumors. To evaluate the molecular features of these tumors, 98 ampullary adenocarcinomas were evaluated and compared to 44 distal bile duct and 18 duodenal adenocarcinomas. Genomic analyses revealed mutations in the WNT signaling pathway among half of the patients and in all three adenocarcinomas irrespective of their origin and histological morphology. These tumors were characterized by a high frequency of inactivating mutations of ELF3, a high rate of microsatellite instability, and common focal deletions and amplifications, suggesting common attributes in the molecular pathogenesis are at play in these tumors. The high frequency of WNT pathway activating mutation, coupled with small-molecule inhibitors of β-catenin in clinical trials, suggests future treatment decisions for these patients may be guided by genomic analysis.

7 Article Antiproliferative effects and mechanisms of liver X receptor ligands in pancreatic ductal adenocarcinoma cells. 2014

Candelaria, Nicholes R / Addanki, Sridevi / Zheng, Jine / Nguyen-Vu, Trang / Karaboga, Husna / Dey, Prasenjit / Gabbi, Chiara / Vedin, Lise-Lotte / Liu, Ka / Wu, Wanfu / Jonsson, Philip K / Lin, Jean Z / Su, Fei / Bollu, Lakshmi Reddy / Hodges, Sally E / McElhany, Amy L / Issazadeh, Mehdi A / Fisher, William E / Ittmann, Michael M / Steffensen, Knut R / Gustafsson, Jan-Åke / Lin, Chin-Yo. ·Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, Houston, Texas, United States of America. · Division of Clinical Chemistry, Department of Laboratory Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden. · Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, Houston, Texas, United States of America; Center for Diabetes Research, Houston Methodist Research Institute, Houston, Texas, United States of America. · Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas, United States of America; The Elkins Pancreas Center at Baylor College of Medicine, Houston, Texas, United States of America. · Department of Pathology and Immunology, Baylor College of Medicine, Houston, Texas, United States of America. · Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, Houston, Texas, United States of America; Department of Biosciences and Nutrition at NOVUM, Karolinska Institutet, Huddinge, Sweden. ·PLoS One · Pubmed #25184494.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is difficult to detect early and is often resistant to standard chemotherapeutic options, contributing to extremely poor disease outcomes. Members of the nuclear receptor superfamily carry out essential biological functions such as hormone signaling and are successfully targeted in the treatment of endocrine-related malignancies. Liver X receptors (LXRs) are nuclear receptors that regulate cholesterol homeostasis, lipid metabolism, and inflammation, and LXR agonists have been developed to regulate LXR function in these processes. Intriguingly, these compounds also exhibit antiproliferative activity in diverse types of cancer cells. In this study, LXR agonist treatments disrupted proliferation, cell-cycle progression, and colony-formation of PDAC cells. At the molecular level, treatments downregulated expression of proteins involved in cell cycle progression and growth factor signaling. Microarray experiments further revealed changes in expression profiles of multiple gene networks involved in biological processes and pathways essential for cell growth and proliferation following LXR activation. These results establish the antiproliferative effects of LXR agonists and potential mechanisms of action in PDAC cells and provide evidence for their potential application in the prevention and treatment of PDAC.