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Pancreatic Neoplasms: HELP
Articles by Liam J. Murray
Based on 6 articles published since 2009
(Why 6 articles?)
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Between 2009 and 2019, L. J. Murray wrote the following 6 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in cancer progression and survival: a systematic review. 2012

Mc Menamin, Úna C / Murray, Liam J / Cantwell, Marie M / Hughes, Carmel M. ·Centre for Public Health, School of Medicine Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast BT12 6BJ, UK. umcmenamin02@qub.ac.uk ·Cancer Causes Control · Pubmed #22116540.

ABSTRACT: OBJECTIVE: To investigate the association between angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) and disease progression and survival in cancer patients. METHODS: Using terms for cancer and ACEIs/ARBs, MEDLINE, EMBASE and Web of Science were systematically searched for observational/interventional studies that used clinically relevant outcomes for cancer progression and survival. RESULTS: Ten studies met the inclusion criteria. Two studies showed a significant improvement in overall survival (OS) with ACEI/ARB use among patients with advanced pancreatic (HR 0.52, 95% CI 0.29-0.88) and non-small cell lung cancer (HR 0.56, 95% CI 0.33-0.95). An improvement in progression-free survival (PFS) was also reported for pancreatic cancer patients (HR 0.58, 95% CI 0.34-0.95) and patients with renal cell carcinoma (HR 0.54, p = 0.02). ACEI/ARB use was protective against breast cancer recurrence (HR 0.60, 95% CI 0.37-0.96), colorectal cancer distant metastasis (OR 0.22, 95% CI 0.08-0.65) and prostate specific antigen (PSA) failure in prostate cancer patients (p = 0.034). One study observed a worse OS (HR 2.01, 95% CI 1.00-4.05) and PFS in ACEI users with multiple myeloma (p = 0.085) while another reported an increased risk of breast cancer recurrence (HR = 1.56, 95% CI 1.02-2.39). CONCLUSION: There is some evidence to suggest that ACEI or ARB use may be associated with improved outcomes in cancer patients. Larger, more robust studies are required to explore this relationship further.

2 Review Can physical activity modulate pancreatic cancer risk? a systematic review and meta-analysis. 2010

O'Rorke, Michael A / Cantwell, Marie M / Cardwell, Chris R / Mulholland, Helen G / Murray, Liam J. ·Cancer Epidemiology Health Services Research Group, Centre for Public Health, Queen's University Belfast, Belfast, Northern Ireland, United Kingdom. mororke04@qub.ac.uk ·Int J Cancer · Pubmed #19856317.

ABSTRACT: Numerous epidemiological studies have examined the association between physical activity and pancreatic cancer; however, findings from individual cohorts have largely not corroborated a protective effect. Among other plausible mechanisms, physical activity may reduce abdominal fat depots inducing metabolic improvements in glucose tolerance and insulin sensitivity, thereby potentially attenuating pancreatic cancer risk. We performed a systematic review to examine associations between physical activity and pancreatic cancer. Six electronic databases were searched from their inception through July 2009, including MEDLINE and EMBASE, seeking observational studies examining any physical activity measure with pancreatic cancer incidence/mortality as an outcome. A random effects model was used to pool individual effect estimates evaluating highest vs. lowest categories of activity. Twenty-eight studies were included. Pooled estimates indicated a reduction in pancreatic cancer risk with higher levels of total (five prospective studies, RR: 0.72, 95% CI: 0.52-0.99) and occupational activity (four prospective studies, RR: 0.75, 95% CI: 0.59-0.96). Nonsignificant inverse associations were seen between risks and recreational and transport physical activity. When examining exercise intensity, moderate activity appeared more protective (RR: 0.79, 95% CI: 0.52-1.20) than vigorous activity (RR: 0.97, 95% CI: 0.85-1.11), but results were not statistically significant and the former activity variable incorporated marked heterogeneity. Despite indications of an inverse relationship with higher levels of work and total activity, there was little evidence of such associations with recreational and other activity exposures.

3 Article Pancreatic cancer and autoimmune diseases: An association sustained by computational and epidemiological case-control approaches. 2019

Gomez-Rubio, Paulina / Piñero, Janet / Molina-Montes, Esther / Gutiérrez-Sacristán, Alba / Marquez, Mirari / Rava, Marta / Michalski, Christoph W / Farré, Antoni / Molero, Xavier / Löhr, Matthias / Perea, José / Greenhalf, William / O'Rorke, Michael / Tardón, Adonina / Gress, Thomas / Barberá, Victor M / Crnogorac-Jurcevic, Tatjana / Muñoz-Bellvís, Luís / Domínguez-Muñoz, Enrique / Balsells, Joaquim / Costello, Eithne / Yu, Jingru / Iglesias, Mar / Ilzarbe, Lucas / Kleeff, Jörg / Kong, Bo / Mora, Josefina / Murray, Liam / O'Driscoll, Damian / Poves, Ignasi / Lawlor, Rita T / Ye, Weimin / Hidalgo, Manuel / Scarpa, Aldo / Sharp, Linda / Carrato, Alfredo / Real, Francisco X / Furlong, Laura I / Malats, Núria / Anonymous2321201. ·Genetic and Molecular Epidemiology Group, Spanish National Cancer Research Center CNIO, Madrid, Spain. · Centro de Investigación Biomédica en Red en Oncología (CIBERONC), Enfermedades Hepáticas y Digestivas (CIBERHD), and Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain. · Research Program on Biomedical Informatics (GRIB), Hospital del Mar Research Institute (IMIM), Universidad Pompeu Fabra (UPF), Barcelona, Spain. · Department of Surgery, Technical University of Munich, Munich, Germany. · Department of Surgery, University of Heidelberg, Heidelberg, Germany. · Department of Gastroenterology, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. · Hospital Universitaru Vall d'Hebron, Exocrine Pancreas Research Unit and Vall d'Hebron Research Institute (VHIR), Barcelona, Spain. · Universitat Auntònoma de Barcelona, Campus de la UAB, Barcelona, Spain. · Department of Clinical Science, Intervention and Technology (CLINTEC), Karolinska Institutet and University Hospital, Stockholm, Sweden. · Department of Surgery, University Hospital 12 de Octubre, Madrid, Spain. · Department of Molecular and Clinical Cancer Medicine, The Royal Liverpool University Hospital, Liverpool, United Kingdom. · Centre for Public Health, Queen's University Belfast, Belfast, United Kingdom. · Department of Medicine, Instituto Universitario de Oncología del Principado de Asturias, Oviedo, Spain. · Department of Gastroenterology, University Hospital of Giessen and Marburg, Marburg, Germany. · Laboratorio de Genética Molecular, Hospital General Universitario de Elche, Elche, Spain. · Centre for Molecular Oncology, John Vane Science Centre, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom. · General and Digestive Surgery Department, Hospital Universitario de Salamanca, Salamanca, Spain. · Department of Gastroenterology, Hospital Clínico Universitario de Santiago de Compostela, Santiago de Compostela, Spain. · Department of Gastroenterology, Hospital del Mar/Parc de Salut Mar, Barcelona, Spain. · Department of Visceral, Vascular and Endocrine Surgery, Martin-Luther-University Halle-Wittenberg, Halle, (Saale), Germany. · Cancer Data Registrars, National Cancer Registry Ireland, Cork, Ireland. · ARC-Net Centre for Applied Research on Cancer, Department of Pathology and Diagnostics, University Hospital Trust of Verona, Verona, Italy. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet and University Hospital, Sweden. · Hospital Madrid-Norte-Sanchinarro and Spanish National Cancer Research Centre (CNIO), Madrid, Spain. · Rosenberg Clinical Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA. · Institute of Health and Society, Newcastle University, Newcastle upon Tyne, United Kingdom. · Department of Oncology, Hospital Ramón y Cajal, Madrid, Spain. · Epithelial Carcinogenesis Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain. · Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra, Barcelona, Spain. · PanGenEU Study Investigators (Additional file 1: Annex S1). ·Int J Cancer · Pubmed #30229903.

ABSTRACT: Deciphering the underlying genetic basis behind pancreatic cancer (PC) and its associated multimorbidities will enhance our knowledge toward PC control. The study investigated the common genetic background of PC and different morbidities through a computational approach and further evaluated the less explored association between PC and autoimmune diseases (AIDs) through an epidemiological analysis. Gene-disease associations (GDAs) of 26 morbidities of interest and PC were obtained using the DisGeNET public discovery platform. The association between AIDs and PC pointed by the computational analysis was confirmed through multivariable logistic regression models in the PanGen European case-control study population of 1,705 PC cases and 1,084 controls. Fifteen morbidities shared at least one gene with PC in the DisGeNET database. Based on common genes, several AIDs were genetically associated with PC pointing to a potential link between them. An epidemiologic analysis confirmed that having any of the nine AIDs studied was significantly associated with a reduced risk of PC (Odds Ratio (OR) = 0.74, 95% confidence interval (CI) 0.58-0.93) which decreased in subjects having ≥2 AIDs (OR = 0.39, 95%CI 0.21-0.73). In independent analyses, polymyalgia rheumatica, and rheumatoid arthritis were significantly associated with low PC risk (OR = 0.40, 95%CI 0.19-0.89, and OR = 0.73, 95%CI 0.53-1.00, respectively). Several inflammatory-related morbidities shared a common genetic component with PC based on public databases. These molecular links could shed light into the molecular mechanisms underlying PC development and simultaneously generate novel hypotheses. In our study, we report sound findings pointing to an association between AIDs and a reduced risk of PC.

4 Article Proton pump inhibitors and histamine-2-receptor antagonists and pancreatic cancer risk: a nested case-control study. 2012

Bradley, M C / Murray, L J / Cantwell, M M / Hughes, C M. ·Clinical and Practice Research Group, School of Pharmacy, Queen's University Belfast, 97 Lisburn Road, Belfast, Northern Ireland BT9 7BL, UK. marie.bradley@qub.ac.uk ·Br J Cancer · Pubmed #22108522.

ABSTRACT: BACKGROUND: The relationship between use of proton pump inhibitors (PPIs) and histamine-2-receptor antagonists (H(2)RAs) and pancreatic cancer risk has yet to be examined. Data from a range of studies suggest biologically plausible mechanisms, whereby these drugs (or the conditions for which they are prescribed) may affect pancreatic cancer risk. The objective of this study was to investigate the relationship between use of PPIs/H(2)RAs and pancreatic cancer risk. METHODS: A nested case-control study was conducted within the UK general practice research database (GPRD). Cases had a diagnosis of exocrine pancreatic cancer and controls were matched to cases on general practice site, sex and year of birth. Exposure to PPIs and to H(2)RAs since entry into GPRD until 2 years before the diagnosis date (corresponding date in controls) and in the 5 years before the diagnosis date were separately assessed. Conditional logistic regression analyses were used to generate odds ratios (ORs) and 95% confidence intervals (CIs) associated with PPI or H(2)RA use compared with nonuse. RESULTS: Ever use of PPIs since entry into the GPRD (excluding the 2 years prior to diagnosis) was not associated with risk of pancreatic cancer; OR (95% CI) 1.02 (0.85-1.22). Neither the dose nor the duration of PPI or H(2)RA use was associated with pancreatic cancer risk. No consistent patterns of association were seen when cumulative exposure (dose and duration) to these drugs was examined separately or together. CONCLUSION: PPI/H(2)RA use, in a UK population, was not associated with pancreatic cancer risk.

5 Article Statins and pancreatic cancer risk: a nested case-control study. 2010

Bradley, Marie C / Hughes, Carmel M / Cantwell, Marie M / Murray, Liam J. ·Clinical and Practice Research Group, School of Pharmacy, Queen's University Belfast, 97 Lisburn Road, Belfast BT9 7BL, Northern Ireland, UK. marie.bradley@qub.ac.uk ·Cancer Causes Control · Pubmed #20697797.

ABSTRACT: OBJECTIVE: To investigate the relationship between statin use and pancreatic cancer risk. METHODS: A nested case-control study was conducted within the UK GPRD. Cases had a diagnosis of primary malignant neoplasia of the exocrine pancreas. Controls were matched with cases on general practice site, sex and year of birth. Exposure of interest was exposure to statins since entry into the GPRD until 1 year before the case diagnosis date. Conditional logistic regression analyses were used to generate ORs and 95% CI associated with statin use compared to non-use. RESULTS: A total of 1,141 pancreatic cancer cases and 7,954 controls were identified. Any use of a statin since entry into the GPRD (excluding the year prior to diagnosis) was not associated with the risk of pancreatic cancer OR 0.93 (95% CI, 0.76-1.14). Neither dose nor duration of statin use affected pancreatic cancer risk. When dose and duration of statin use combined were assessed, no evidence of reduced risk was seen for long-term users of high-dose statins OR 0.71 (0.42-1.20). Statin type (simvastatin vs atorvastatin) was not associated with pancreatic cancer risk. CONCLUSION: Statin use at doses for managing hypercholesterolaemia, in a UK population, was not associated with the risk of exocrine pancreatic cancer.

6 Article Non-steroidal anti-inflammatory drugs and pancreatic cancer risk: a nested case-control study. 2010

Bradley, M C / Hughes, C M / Cantwell, M M / Napolitano, G / Murray, L J. ·Cancer Epidemiology and Prevention Research Group, Centre for Public Health, Queen's University, Mulhouse Building, Royal Victoria Hospital, Belfast BT12 6BJ, Northern Ireland, UK. ·Br J Cancer · Pubmed #20372155.

ABSTRACT: BACKGROUND: Non-steroidal anti-inflammatory drug (NSAID) use has been linked with pancreatic cancer risk; however, findings from epidemiological studies are inconsistent. METHODS: A nested case-control study was conducted within the UK General Practice Research Database. Cases (n=1141) had a diagnosis of primary cancer of the exocrine pancreas between January 1995 and June 2006. Controls (n=7954) were matched with each case on general practice site, sex and year of birth. Conditional logistic regression analyses were used to generate odds ratios (OR) and 95% confidence intervals (CI) associated with NSAID use compared with non-use. RESULTS: Any use of NSAID in the 5 years before the index date or since entry into the database (excluding the year before diagnosis) was not associated with risk of pancreatic cancer; OR 0.96 (95% CI, 0.84-1.10) and 1.03 (95% CI 0.89-1.19), respectively. Exposure to NSAIDs for > 773 days, in the 5 years pre-diagnosis, was associated with a reduced risk of pancreatic cancer OR 0.78 (95%CI 0.62-0.97). There was evidence of reduced pancreatic cancer risk with long-term use (5 years or more) of lower doses of NSAIDs OR 0.70 (95% CI 0.49-0.99). CONCLUSION: Long-term exposure to NSAIDs may be associated with a reduction in risk of pancreatic cancer.