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Genetic Polymorphisms Involved in Mitochondrial Metabolism and Pancreatic Cancer Risk
G. Peduzzi, M. Gentiluomo, F. Tavano, PG. Arcidiacono, S. Ermini, P. Vodicka, U. Boggi, GM. Cavestro, G. Capurso, L. Morelli, AC. Milanetto, R. Pezzilli, RT. Lawlor, S. Carrara, M. Lovecek, P. Souček, F. Guo, T. Hackert, FG. Uzunoğlu, M. Gazouli,...
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Free Medical Journals
from 1991 to 1 year ago
Freely Accessible Science Journals
from 1991 to 12 months ago
Open Access Digital Library
from 1991-11-01
Open Access Digital Library
from 1991-11-01
- MeSH
- Carcinoma, Pancreatic Ductal genetics metabolism MeSH
- Genetic Variation MeSH
- Genome, Mitochondrial MeSH
- Polymorphism, Single Nucleotide MeSH
- Humans MeSH
- Mitochondria metabolism MeSH
- Pancreatic Neoplasms genetics metabolism MeSH
- Case-Control Studies MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
BACKGROUND: The mitochondrial metabolism has been associated with pancreatic ductal adenocarcinoma (PDAC) risk. Recent evidence also suggests the involvement of the genetic variability of the mitochondrial function in several traits involved in PDAC etiology. However, a systematic investigation of the genetic variability of mitochondrial genome (mtSNP) and of all the nuclear genes involved in its functioning (n-mtSNPs) has never been reported. METHODS: We conducted a two-phase association study of mtSNPs and n-mtSNPs to assess their effect on PDAC risk. We analyzed 35,297 n-mtSNPs and 101 mtSNPs in up to 55,870 individuals (12,884 PDAC cases and 42,986 controls). In addition, we also conducted a gene-based analysis on 1,588 genes involved in mitochondrial metabolism using Multi-marker Analysis of GenoMic Annotation (MAGMA) software. RESULTS: In the discovery phase, we identified 49 n-mtSNPs and no mtSNPs associated with PDAC risk (P < 0.05). In the second phase, none of the findings were replicated. In the gene-level analysis, we observed that three genes (TERT, SUGCT, and SURF1) involved in the mitochondrial metabolism showed an association below the Bonferroni-corrected threshold of statistical significance (P = 0.05/1588 = 3.1 × 10-5). CONCLUSIONS: Even though the mitochondrial metabolism might be involved in PDAC etiology, our results, obtained in a study with one of the largest sample sizes to date, show that neither n-mtSNPs nor mtSNPs are associated with PDAC risk. IMPACT: This large case-control study does not support a role of the genetic variability of the mitochondrial function in PDAC risk.
1st Department of Surgery University Hospital Olomouc Olomouc Czech Republic
ARC NET Centre for Applied Research on Cancer University and Hospital Trust of Verona Verona Italy
Biomedical Center Faculty of Medicine in Pilsen Charles University Pilsen Czech Republic
Centre for Translational Medicine Department of Medicine University of Szeged Szeged Hungary
Clinica Chirurgica 1 Department DISCOG University of Padova Padua Italy
Clinica Chirurgica 3 Department DISCOG University of Padova Padua Italy
Department DIMED University of Padova Padua Italy
Department of Biology University of Pisa Pisa Italy
Department of Digestive Tract Diseases Medical University of Lodz Lodz Poland
Department of Medical Biotechnologies University of Siena Siena Italy
Department of Surgery Erasmus Medical Center Erasmus University Rotterdam the Netherlands
Department of Surgery Unit of Experimental Surgical Pathology Pisa University Hospital Pisa Italy
Division of General and Transplant Surgery Pisa University Hospital Pisa Italy
Division of Preventive Oncology German Cancer Research Center Heidelberg Germany
Endoscopic Unit Department of Gastroenterology IRCCS Humanitas Research Hospital Milan Italy
Former senior scientist Department for Determinants of Chronic Diseases Bilthoven the Netherlands
Fundeni Clinical Institute Bucharest Romania
Gastroenterology Department Lithuanian University of Health Sciences Kaunas Lithuania
Gastroenterology Unit San Carlo Hospital Potenza Italy
Genomic Epidemiology Research Group German Cancer Research Center Heidelberg Germany
German Cancer Consortium Heidelberg Germany
Institute for Digestive Research Lithuanian University of Health Sciences Kaunas Lithuania
Institute for Translational Medicine Medical School University of Pécs Pécs Hungary
Institute of Experimental Medicine Czech Academy of Sciences Prague Czech Republic
Laboratory of Biology Medical School National and Kapodistrian University of Athens Athens Greece
Medical Faculty Heidelberg University of Heidelberg Heidelberg Germany
Pál Heim National Institute of Pediatrics Budapest Hungary
Transfusion Service Azienda Ospedaliero Universitaria Meyer Children's Hospital Florence Italy
References provided by Crossref.org
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- $a Genetic Polymorphisms Involved in Mitochondrial Metabolism and Pancreatic Cancer Risk / $c G. Peduzzi, M. Gentiluomo, F. Tavano, PG. Arcidiacono, S. Ermini, P. Vodicka, U. Boggi, GM. Cavestro, G. Capurso, L. Morelli, AC. Milanetto, R. Pezzilli, RT. Lawlor, S. Carrara, M. Lovecek, P. Souček, F. Guo, T. Hackert, FG. Uzunoğlu, M. Gazouli, A. Párniczky, J. Kupcinskas, MF. Bijlsma, B. Bueno-de-Mesquita, R. Vermeulen, CHJ. van Eijck, K. Jamroziak, R. Talar-Wojnarowska, W. Greenhalf, D. Gioffreda, MC. Petrone, S. Landi, L. Archibugi, M. Puzzono, N. Funel, C. Sperti, ML. Piredda, B. Mohelnikova-Duchonova, Y. Lu, V. Hlaváč, X. Gao, M. Schneider, JR. Izbicki, G. Theodoropoulos, S. Bunduc, E. Kreivenaite, OR. Busch, E. Małecka-Panas, E. Costello, F. Perri, SGG. Testoni, G. Vanella, C. Pasquali, M. Oliverius, H. Brenner, M. Loos, M. Götz, K. Georgiou, B. Erőss, E. Maiello, A. Szentesi, F. Bazzocchi, D. Basso, JP. Neoptolemos, P. Hegyi, V. Kiudelis, F. Canzian, D. Campa
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