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Pancreatic Neoplasms: HELP
Articles by Celia M. T. Greenwood
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Celia Greenwood wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article A region-based gene association study combined with a leave-one-out sensitivity analysis identifies SMG1 as a pancreatic cancer susceptibility gene. 2019

Wong, Cavin / Chen, Fei / Alirezaie, Najmeh / Wang, Yifan / Cuggia, Adeline / Borgida, Ayelet / Holter, Spring / Lenko, Tatiana / Domecq, Celine / Anonymous2511041 / Petersen, Gloria M / Syngal, Sapna / Brand, Randall / Rustgi, Anil K / Cote, Michele L / Stoffel, Elena / Olson, Sara H / Roberts, Nicholas J / Akbari, Mohammad R / Majewski, Jacek / Klein, Alison P / Greenwood, Celia M T / Gallinger, Steven / Zogopoulos, George. ·The Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada. · The Goodman Cancer Research Centre of McGill University, Montreal, Quebec, Canada. · Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America. · McGill University and Genome Quebec Innovation Centre, Montreal, Quebec, Canada. · Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada. · Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, United States of America. · Division of Cancer Genetics and Prevention, Dana-Farber Cancer Institute, Gastroenterology Division, Brigham and Women's Hospital, Harvard Medical Schozol, Boston, Massachusetts, United States of America. · Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America. · Division of Gastroenterology, Departments of Medicine and Genetics, Pancreatic Cancer Translation Center of Excellence, Abramson Cancer Center, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States of America. · Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan, United States of America. · Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States of America. · Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America. · Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland, United States of America. · The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University, Baltimore, Maryland, United States of America. · Women's College Hospital Research Institute, Women's College Hospital, Toronto, Ontario, Canada. · Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada. · Ludmer Centre for Neuroinformatics & Mental Health, McGill University, Montreal, Quebec, Canada. · Lady Davis Institute, Jewish General Hospital, McGill University, Montreal, Quebec, Canada. · Gerald Bronfman Department of Oncology, and Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montreal, Quebec, Canada. ·PLoS Genet · Pubmed #31469826.

ABSTRACT: Pancreatic adenocarcinoma (PC) is a lethal malignancy that is familial or associated with genetic syndromes in 10% of cases. Gene-based surveillance strategies for at-risk individuals may improve clinical outcomes. However, familial PC (FPC) is plagued by genetic heterogeneity and the genetic basis for the majority of FPC remains elusive, hampering the development of gene-based surveillance programs. The study was powered to identify genes with a cumulative pathogenic variant prevalence of at least 3%, which includes the most prevalent PC susceptibility gene, BRCA2. Since the majority of known PC susceptibility genes are involved in DNA repair, we focused on genes implicated in these pathways. We performed a region-based association study using the Mixed-Effects Score Test, followed by leave-one-out characterization of PC-associated gene regions and variants to identify the genes and variants driving risk associations. We evaluated 398 cases from two case series and 987 controls without a personal history of cancer. The first case series consisted of 109 patients with either FPC (n = 101) or PC at ≤50 years of age (n = 8). The second case series was composed of 289 unselected PC cases. We validated this discovery strategy by identifying known pathogenic BRCA2 variants, and also identified SMG1, encoding a serine/threonine protein kinase, to be significantly associated with PC following correction for multiple testing (p = 3.22x10-7). The SMG1 association was validated in a second independent series of 532 FPC cases and 753 controls (p<0.0062, OR = 1.88, 95%CI 1.17-3.03). We showed segregation of the c.4249A>G SMG1 variant in 3 affected relatives in a FPC kindred, and we found c.103G>A to be a recurrent SMG1 variant associating with PC in both the discovery and validation series. These results suggest that SMG1 is a novel PC susceptibility gene, and we identified specific SMG1 gene variants associated with PC risk.

2 Article Association between Variants in Atopy-Related Immunologic Candidate Genes and Pancreatic Cancer Risk. 2015

Cotterchio, Michelle / Lowcock, Elizabeth / Bider-Canfield, Zoe / Lemire, Mathieu / Greenwood, Celia / Gallinger, Steven / Hudson, Thomas. ·Prevention and Cancer Control, Cancer Care Ontario, Toronto, ON M5G 2L7, Canada; Dalla Lana School of Public Health, University of Toronto, Toronto, ON M5T 3M7, Canada. · Prevention and Cancer Control, Cancer Care Ontario, Toronto, ON M5G 2L7, Canada. · Ontario Institute for Cancer Research, Toronto, ON M5G 0A3, Canada. · Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC H3T 1E2, Canada. · Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON M5G 1X5, Canada; Division of General Surgery, Toronto General Hospital, Toronto, ON M5G 2C4, Canada. · Ontario Institute for Cancer Research, Toronto, ON M5G 0A3, Canada; Department of Molecular Genetics, University of Toronto, Toronto, ON M5S 1A1, Canada. ·PLoS One · Pubmed #25945796.

ABSTRACT: BACKGROUND: Many epidemiology studies report that atopic conditions such as allergies are associated with reduced pancreas cancer risk. The reason for this relationship is not yet understood. This is the first study to comprehensively evaluate the association between variants in atopy-related candidate genes and pancreatic cancer risk. METHODS: A population-based case-control study of pancreas cancer cases diagnosed during 2011-2012 (via Ontario Cancer Registry), and controls recruited using random digit dialing utilized DNA from 179 cases and 566 controls. Following an exhaustive literature review, SNPs in 180 candidate genes were pre-screened using dbGaP pancreas cancer GWAS data; 147 SNPs in 56 allergy-related immunologic genes were retained and genotyped. Logistic regression was used to estimate age-adjusted odd ratio (AOR) for each variant and false discovery rate was used to adjust Wald p-values for multiple testing. Subsequently, a risk allele score was derived based on statistically significant variants. RESULTS: 18 SNPs in 14 candidate genes (CSF2, DENND1B, DPP10, FLG, IL13, IL13RA2, LRP1B, NOD1, NPSR1, ORMDL3, RORA, STAT4, TLR6, TRA) were significantly associated with pancreas cancer risk. After adjustment for multiple comparisons, two LRP1B SNPs remained statistically significant; for example, LRP1B rs1449477 (AA vs. CC: AOR=0.37, 95% CI: 0.22-0.62; p (adjusted)=0.04). Furthermore, the risk allele score was associated with a significant reduction in pancreas cancer risk (p=0.0007). CONCLUSIONS: Preliminary findings suggest certain atopy-related variants may be associated with pancreas cancer risk. Further studies are needed to replicate this, and to elucidate the biology behind the growing body of epidemiologic evidence suggesting allergies may reduce pancreatic cancer risk.

3 Article Association between allergies and risk of pancreatic cancer. 2014

Cotterchio, Michelle / Lowcock, Elizabeth / Hudson, Thomas J / Greenwood, Celia / Gallinger, Steven. ·Authors' Affiliations: Prevention and Cancer Control, Cancer Care Ontario; Dalla Lana School of Public Health, University of Toronto; Departments of Medical Biophysics and Molecular Genetics, University of Toronto; Ontario Institute for Cancer Research; Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital; and Division of General Surgery, Toronto General Hospital, Toronto, Ontario; and Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Canada. ·Cancer Epidemiol Biomarkers Prev · Pubmed #24554712.

ABSTRACT: BACKGROUND: Less than 10% of pancreatic cancer cases survive 5 years, yet its etiology is not well understood. Studies suggest allergies are associated with reduced pancreatic cancer risk. Our study collected additional information on allergies (including skin prick test results and differentiation of allergic/nonallergic asthma), and is the first to assess possible confounding by allergy medications. METHODS: A population-based case-control study was designed to comprehensively assess the association between allergy and pancreatic cancer risk. Pancreas cancer cases were diagnosed during 2011 to 2012, and identified through the Ontario Cancer Registry (345 cases). Population-based controls were identified using random digit dialing and age/sex frequency matched to cases (1,285 controls). Questionnaires collected lifetime allergy history (type of allergy, age at onset, skin prick testing results), allergy medications, and established pancreas cancer risk factors. Logistic regression was used to estimate odd ratios and test potential confounders, including allergy medications. RESULTS: Hay fever was associated with a significant reduction in pancreatic cancer risk [AOR = 0.68; 95% confidence intervals (CI), 0.52-0.89], and reduction was greatest for those whose skin prick test was positive for hay fever allergens. No particular patterns were observed as regards age at onset and duration of allergy. Positive dust/mold allergy skin prick test and animal allergies were associated with a statistically significant reduced pancreatic cancer risk; AOR = 0.49; 95% CI, 0.31-0.78 and AOR = 0.68; 95% CI, 0.46-0.99, respectively. Asthma was not associated with pancreatic cancer risk. CONCLUSIONS/IMPACT: These findings support the growing body of evidence that suggests certain allergies are associated with reduced pancreatic cancer risk.