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6 results on '"Oliverius, M."'

1. Do pancreatic cancer and chronic pancreatitis share the same genetic risk factors? A PANcreatic Disease ReseArch (PANDoRA) consortium investigation

Author

Campa, D, Pastore, M, Capurso, G, Hackert, T, Di Leo, M, Izbicki, JR, Khaw, K-T, Gioffreda, D, Kupcinskas, J, Pasquali, C, Macinga, P, Kaaks, R, Stigliano, S, Peeters, PH, Key, TJ, Talar-Wojnarowska, R, Vodicka, P, Valente, R, Vashist, YK, Salvia, R, Papaconstantinou, I, Shimizu, Y, Valsuani, C, Zambon, CF, Gazouli, M, Valantiene, I, Niesen, W, Mohelnikova-Duchonova, B, Hara, K, Soucek, P, Malecka-Panas, E, Bueno-de-Mesquita, HBA, Johnson, T, Brenner, H, Tavano, F, Fogar, P, Ito, H, Sperti, C, Butterbach, K, Latiano, A, Andriulli, A, Cavestro, GM, Busch, ORC, Dijk, F, Greenhalf, W, Matsuo, K, Lombardo, C, Strobel, O, König, A-K, Cuk, K, Strothmann, H, Katzke, V, Cantore, M, Mambrini, A, Oliverius, M, Pezzilli, R, Landi, S, Canzian, F, Other departments, CCA - Imaging and biomarkers, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, Campa, Daniele, Pastore, Manuela, Capurso, Gabriele, Hackert, Thilo, Di Leo, Milena, Izbicki, Jakob R, Khaw, Kay tee, Gioffreda, Domenica, Kupcinskas, Juoza, Pasquali, Claudio, Macinga, Peter, Kaaks, Rudolf, Stigliano, Serena, Peeters, Petra H, Key, Timothy J, Talar wojnarowska, Renata, Vodicka, Pavel, Valente, Roberto, Vashist, Yogesh K, Salvia, Roberto, Papaconstantinou, Ioanni, Shimizu, Yasuhiro, Valsuani, Chiara, Zambon, Carlo Federico, Gazouli, Maria, Valantiene, Irena, Niesen, Willem, Mohelnikova duchonova, Beatrice, Hara, Kazuo, Soucek, Pavel, Malecka panas, Ewa, Bueno de mesquita, H. Ba, Johnson, Theron, Brenner, Herman, Tavano, Francesca, Fogar, Paola, Ito, Hidemi, Sperti, Cosimo, Butterbach, Katja, Latiano, Anna, Andriulli, Angelo, Cavestro, GIULIA MARTINA, Busch, Olivier R. C, Dijk, Frederike, Greenhalf, William, Matsuo, Keitaro, Lombardo, Carlo, Strobel, Oliver, König, Anna katharina, Cuk, Katarina, Strothmann, Hendrik, Katzke, Verena, Cantore, Maurizio, Mambrini, Andrea, Oliverius, Martin, Pezzilli, Raffaele, Landi, Stefano, and Canzian, Federico

Subjects
Adult, Male, Cancer Research, endocrine system diseases, Chronic pancreatiti, pancreatic ductal adenocarcinoma, Adenocarcinoma, Polymorphism, Single Nucleotide, genetic polymorphisms, Risk Factors, Pancreatitis, Chronic, Biomarkers, Tumor, genetic polymorphism, Humans, Trypsin, Chronic, Polymorphism, Aged, Retrospective Studies, Tumor, Carcinoma, association, Nuclear Proteins, Single Nucleotide, Middle Aged, ACUTE PANCREATITIS, Prognosis, digestive system diseases, PANCREATIC CANCER, Pancreatic Neoplasms, Pancreatitis, Oncology, Pancreatic Ductal, Case-Control Studies, Chronic pancreatitis, Carcinoma, Pancreatic Ductal, Female, Follow-Up Studies, Trypsinogen, Biomarkers
Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a very aggressive tumor with a five-year survival of less than 6%. Chronic pancreatitis (CP), an inflammatory process in of the pancreas, is a strong risk factor for PDAC. Several genetic polymorphisms have been discovered as susceptibility loci for both CP and PDAC. Since CP and PDAC share consistent number of epidemiologic risk factors, the aim of this study was to investigate whether specific CP risk loci also contribute to PDAC susceptibility. We selected five common SNPs (rs11988997, rs379742, rs10273639 rs2995271 and rs12688220) that were identified as susceptibility markers for CP and analyzed them in 2,914 PDAC cases, 356 CP cases and 5,596 controls retrospectively collected in the context of the international PANDoRA consortium. We found a weak association between the minor allele of the PRSS1-PRSS2-rs10273639 and an increased risk of developing PDAC (ORhomozygous =1.19, 95% CI 1.02-1.38, p=0.023). Additionally all the SNPs confirmed statistically significant associations with risk of developing CP, the strongest being PRSS1-PRSS2-rs10273639 (ORheterozygous =0.51, 95% CI 0.39-0.67, p=1.10x10(-6) ) and MORC4-rs 12837024 (ORhomozygous =2.07 (1.55-2.77, ptrend =0.7x10(-11) ). Taken together, the results from our study do not support variants rs11988997, rs379742, rs10273639 rs2995271 and rs12688220 as strong predictors of PDAC risk, but further support the role of these SNPs in CP susceptibility. Our study suggests that CP and PDAC probably do not share genetic susceptibility, at least in terms of high frequency variants. This article is protected by copyright. All rights reserved.

Published
2017

2. Potential association between PSCA rs2976395 functional variant and pancreatic cancer risk.

Author

Corradi C, Lencioni G, Felici A, Rizzato C, Gentiluomo M, Ermini S, Archibugi L, Mickevicius A, Lucchesi M, Malecka-Wojciesko E, Basso D, Arcidiacono PG, Petrone MC, Carrara S, Götz M, Bunduc S, Holleczek B, Aoki MN, Uzunoglu FG, Zanette DL, Mambrini A, Jamroziak K, Oliverius M, Lovecek M, Cavestro GM, Milanetto AC, Peduzzi G, Duchonova BM, Izbicki JR, Zalinkevicius R, Hlavac V, van Eijck CHJ, Brenner H, Vanella G, Vokacova K, Soucek P, Tavano F, Perri F, Capurso G, Hussein T, Kiudelis M, Kupcinskas J, Busch OR, Morelli L, Theodoropoulos GE, Testoni SGG, Adamonis K, Neoptolemos JP, Gazouli M, Pasquali C, Kormos Z, Skalicky P, Pezzilli R, Sperti C, Kauffmann E, Büchler MW, Schöttker B, Hegyi P, Capretti G, Lawlor RT, Canzian F, and Campa D

Subjects
Humans, Male, Case-Control Studies, White People genetics, Female, Quantitative Trait Loci, Alleles, Asian People genetics, Middle Aged, Polymorphism, Single Nucleotide, Pancreatic Neoplasms genetics, Genetic Predisposition to Disease, DNA Methylation, Carcinoma, Pancreatic Ductal genetics, GPI-Linked Proteins genetics, Linkage Disequilibrium, Antigens, Neoplasm genetics, Neoplasm Proteins genetics
Abstract

Correlated regions of systemic interindividual variation (CoRSIV) represent a small proportion of the human genome showing DNA methylation patterns that are the same in all human tissues, are different among individuals, and are partially regulated by genetic variants in cis. In this study we aimed at investigating single-nucleotide polymorphisms (SNPs) within CoRSIVs and their involvement with pancreatic ductal adenocarcinoma (PDAC) risk. We analyzed 29,099 CoRSIV-SNPs and 133,615 CoRSIV-mQTLs in 14,394 cases and 247,022 controls of European and Asian descent. We observed that the A allele of the rs2976395 SNP was associated with increased PDAC risk in Europeans (p = 2.81 × 10 -5 ). This SNP lies in the prostate stem cell antigen gene and is in perfect linkage disequilibrium with a variant (rs2294008) that has been reported to be associated with risk of many other cancer types. The A allele is associated with the DNA methylation level of the gene according to the PanCan-meQTL database and with overexpression according to QTLbase. The expression of the gene has been observed to be deregulated in many tumors of the gastrointestinal tract including pancreatic cancer; however, functional studies are needed to elucidate the function relevance of the association., (© 2024 UICC.)

Published
2024
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3. Polymorphisms within autophagy-related genes as susceptibility biomarkers for pancreatic cancer: A meta-analysis of three large European cohorts and functional characterization.

Author

Gálvez-Montosa F, Peduzzi G, Sanchez-Maldonado JM, Ter Horst R, Cabrera-Serrano AJ, Gentiluomo M, Macauda A, Luque N, Ünal P, García-Verdejo FJ, Li Y, López López JA, Stein A, Bueno-de-Mesquita HB, Arcidiacono PG, Zanette DL, Kahlert C, Perri F, Soucek P, Talar-Wojnarowska R, Theodoropoulos GE, Izbicki JR, Tamás H, Van Laarhoven H, Nappo G, Petrone MC, Lovecek M, Vermeulen RCH, Adamonis K, Reyes-Zurita FJ, Holleczek B, Sumskiene J, Mohelníková-Duchoňová B, Lawlor RT, Pezzilli R, Aoki MN, Pasquali C, Petrenkiene V, Basso D, Bunduc S, Comandatore A, Brenner H, Ermini S, Vanella G, Goetz MR, Archibugi L, Lucchesi M, Uzunoglu FG, Busch O, Milanetto AC, Puzzono M, Kupcinskas J, Morelli L, Sperti C, Carrara S, Capurso G, van Eijck CHJ, Oliverius M, Roth S, Tavano F, Kaaks R, Szentesi A, Vodickova L, Luchini C, Schöttker B, Landi S, Dohan O, Tacelli M, Greenhalf W, Gazouli M, Neoptolemos JP, Cavestro GM, Boggi U, Latiano A, Hegyi P, Ginocchi L, Netea MG, Sánchez-Rovira P, Canzian F, Campa D, and Sainz J

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with patients having unresectable or metastatic disease at diagnosis, with poor prognosis and very short survival. Given that genetic variation within autophagy-related genes influences autophagic flux and susceptibility to solid cancers, we decided to investigate whether 55,583 single nucleotide polymorphisms (SNPs) within 234 autophagy-related genes could influence the risk of developing PDAC in three large independent cohorts of European ancestry including 12,754 PDAC cases and 324,926 controls. The meta-analysis of these populations identified, for the first time, the association of the BID rs9604789 variant with an increased risk of developing the disease (OR Meta  = 1.31, p = 9.67 × 10 -6 ). We also confirmed the association of TP63 rs1515496 and TP63 rs35389543 variants with PDAC risk (OR = 0.89, p = 6.27 × 10 -8 and OR = 1.16, p = 2.74 × 10 -5 ). Although it is known that BID induces autophagy and TP63 promotes cell growth, cell motility and invasion, we also found that carriers of the TP63 rs1515496G allele had increased numbers of FOXP3+ Helios+ T regulatory cells and CD45RA+ T regulatory cells (p = 7.67 × 10 -4 and p = 1.56 × 10 -3 ), but also decreased levels of CD4+ T regulatory cells (p = 7.86 × 10 -4 ). These results were in agreement with research suggesting that the TP63 rs1515496 variant alters binding sites for FOXA1 and CTCF, which are transcription factors involved in modulating specific subsets of regulatory T cells. In conclusion, this study identifies BID as new susceptibility locus for PDAC and confirms previous studies suggesting that the TP63 gene is involved in the development of PDAC. This study also suggests new pathogenic mechanisms of the TP63 locus in PDAC., (© 2024 The Author(s). International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.)

Published
2024
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4. Genome-wide scan of long noncoding RNA single nucleotide polymorphisms and pancreatic cancer susceptibility.

Author

Corradi C, Gentiluomo M, Gajdán L, Cavestro GM, Kreivenaite E, Di Franco G, Sperti C, Giaccherini M, Petrone MC, Tavano F, Gioffreda D, Morelli L, Soucek P, Andriulli A, Izbicki JR, Napoli N, Małecka-Panas E, Hegyi P, Neoptolemos JP, Landi S, Vashist Y, Pasquali C, Lu Y, Cervena K, Theodoropoulos GE, Moz S, Capurso G, Strobel O, Carrara S, Hackert T, Hlavac V, Archibugi L, Oliverius M, Vanella G, Vodicka P, Arcidiacono PG, Pezzilli R, Milanetto AC, Lawlor RT, Ivanauskas A, Szentesi A, Kupcinskas J, Testoni SGG, Lovecek M, Nentwich M, Gazouli M, Luchini C, Zuppardo RA, Darvasi E, Brenner H, Gheorghe C, Jamroziak K, Canzian F, and Campa D

Subjects
Aged, Case-Control Studies, Computational Biology methods, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Middle Aged, Carcinoma, Pancreatic Ductal genetics, Cyclin-Dependent Kinase Inhibitor p15 genetics, MicroRNAs genetics, Pancreatic Neoplasms genetics, Polymorphism, Single Nucleotide, RNA, Long Noncoding genetics
Abstract

Pancreatic ductal adenocarcinoma (PDAC) is projected to become the second cancer-related cause of death by 2030. Identifying novel risk factors, including genetic risk loci, could be instrumental in risk stratification and implementation of prevention strategies. Long noncoding RNAs (lncRNAs) are involved in regulation of key biological processes, and the possible role of their genetic variability has been unexplored so far. Combining genome wide association studies and functional data, we investigated the genetic variability in all lncRNAs. We analyzed 9893 PDAC cases and 9969 controls and identified a genome-wide significant association between the rs7046076 SNP and risk of developing PDAC (P = 9.73 × 10 -9 ). This SNP is located in the NONHSAG053086.2 (lnc-SMC2-1) gene and the risk allele is predicted to disrupt the binding of the lncRNA with the micro-RNA (miRNA) hsa-mir-1256 that regulates several genes involved in cell cycle, such as CDKN2B. The CDKN2B region is pleiotropic and its genetic variants have been associated with several human diseases, possibly though an imperfect interaction between lncRNA and miRNA. We present a novel PDAC risk locus, supported by a genome-wide statistical significance and a plausible biological mechanism., (© 2021 UICC.)

Published
2021
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5. Genome-wide association study identifies an early onset pancreatic cancer risk locus.

Author

Campa D, Gentiluomo M, Obazee O, Ballerini A, Vodickova L, Hegyi P, Soucek P, Brenner H, Milanetto AC, Landi S, Gao X, Bozzato D, Capurso G, Tavano F, Vashist Y, Hackert T, Bambi F, Bursi S, Oliverius M, Gioffreda D, Schöttker B, Ivanauskas A, Mohelnikova-Duchonova B, Darvasi E, Pezzilli R, Małecka-Panas E, Strobel O, Gazouli M, Katzke V, Szentesi A, Cavestro GM, Farkas G Jr, Izbicki JR, Moz S, Archibugi L, Hlavac V, Vincze Á, Talar-Wojnarowska R, Rusev B, Kupcinskas J, Greenhalf B, Dijk F, Giese N, Boggi U, Andriulli A, Busch OR, Vanella G, Vodicka P, Nentwich M, Lawlor RT, Theodoropoulos GE, Jamroziak K, Zuppardo RA, Moletta L, Ginocchi L, Kaaks R, Neoptolemos JP, Lucchesi M, and Canzian F

Subjects
Carcinoma, Pancreatic Ductal genetics, Carcinoma, Pancreatic Ductal pathology, Case-Control Studies, Female, Genome-Wide Association Study methods, Humans, Male, Middle Aged, Pancreas pathology, Pancreatic Neoplasms pathology, Polymorphism, Single Nucleotide genetics, Risk Factors, Pancreatic Neoplasms, Genetic Predisposition to Disease genetics, Pancreatic Neoplasms genetics
Abstract

Early onset pancreatic cancer (EOPC) is a rare disease with a very high mortality rate. Almost nothing is known on the genetic susceptibility of EOPC, therefore, we performed a genome-wide association study (GWAS) to identify novel genetic variants specific for patients diagnosed with pancreatic ductal adenocarcinoma (PDAC) at younger ages. In the first phase, conducted on 821 cases with age of onset ≤60 years, of whom 198 with age of onset ≤50, and 3227 controls from PanScan I-II, we observed four SNPs (rs7155613, rs2328991, rs4891017 and rs12610094) showing an association with EOPC risk (P < 1 × 10 -4 ). We replicated these SNPs in the PANcreatic Disease ReseArch (PANDoRA) consortium and used additional in silico data from PanScan III and PanC4. Among these four variants rs2328991 was significant in an independent set of 855 cases with age of onset ≤60 years, of whom 265 with age of onset ≤50, and 4142 controls from the PANDoRA consortium while in the in silico data, we observed no statistically significant association. However, the resulting meta-analysis supported the association (P = 1.15 × 10 -4 ). In conclusion, we propose a novel variant rs2328991 to be involved in EOPC risk. Even though it was not possible to find a mechanistic link between the variant and the function, the association is supported by a solid statistical significance obtained in the largest study on EOPC genetics present so far in the literature., (© 2020 UICC.)

Published
2020
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6. Do pancreatic cancer and chronic pancreatitis share the same genetic risk factors? A PANcreatic Disease ReseArch (PANDoRA) consortium investigation.

Author

Campa D, Pastore M, Capurso G, Hackert T, Di Leo M, Izbicki JR, Khaw KT, Gioffreda D, Kupcinskas J, Pasquali C, Macinga P, Kaaks R, Stigliano S, Peeters PH, Key TJ, Talar-Wojnarowska R, Vodicka P, Valente R, Vashist YK, Salvia R, Papaconstantinou I, Shimizu Y, Valsuani C, Zambon CF, Gazouli M, Valantiene I, Niesen W, Mohelnikova-Duchonova B, Hara K, Soucek P, Malecka-Panas E, Bueno-de-Mesquita HBA, Johnson T, Brenner H, Tavano F, Fogar P, Ito H, Sperti C, Butterbach K, Latiano A, Andriulli A, Cavestro GM, Busch ORC, Dijk F, Greenhalf W, Matsuo K, Lombardo C, Strobel O, König AK, Cuk K, Strothmann H, Katzke V, Cantore M, Mambrini A, Oliverius M, Pezzilli R, Landi S, and Canzian F

Subjects
Adenocarcinoma genetics, Adenocarcinoma pathology, Adult, Aged, Carcinoma, Pancreatic Ductal pathology, Case-Control Studies, Female, Follow-Up Studies, Humans, Male, Middle Aged, Nuclear Proteins genetics, Pancreatic Neoplasms pathology, Pancreatitis, Chronic pathology, Prognosis, Retrospective Studies, Risk Factors, Trypsin genetics, Trypsinogen genetics, Biomarkers, Tumor genetics, Carcinoma, Pancreatic Ductal genetics, Pancreatic Neoplasms genetics, Pancreatitis, Chronic genetics, Polymorphism, Single Nucleotide
Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a very aggressive tumor with a five-year survival of less than 6%. Chronic pancreatitis (CP), an inflammatory process in of the pancreas, is a strong risk factor for PDAC. Several genetic polymorphisms have been discovered as susceptibility loci for both CP and PDAC. Since CP and PDAC share a consistent number of epidemiologic risk factors, the aim of this study was to investigate whether specific CP risk loci also contribute to PDAC susceptibility. We selected five common SNPs (rs11988997, rs379742, rs10273639, rs2995271 and rs12688220) that were identified as susceptibility markers for CP and analyzed them in 2,914 PDAC cases, 356 CP cases and 5,596 controls retrospectively collected in the context of the international PANDoRA consortium. We found a weak association between the minor allele of the PRSS1-PRSS2-rs10273639 and an increased risk of developing PDAC (OR homozygous  = 1.19, 95% CI 1.02-1.38, p = 0.023). Additionally all the SNPs confirmed statistically significant associations with risk of developing CP, the strongest being PRSS1-PRSS2-rs10273639 (OR heterozygous  = 0.51, 95% CI 0.39-0.67, p = 1.10 × 10 -6 ) and MORC4-rs 12837024 (OR homozygous  = 2.07 (1.55-2.77, p trend  = 0.7 × 10 -11 ). Taken together, the results from our study do not support variants rs11988997, rs379742, rs10273639, rs2995271 and rs12688220 as strong predictors of PDAC risk, but further support the role of these SNPs in CP susceptibility. Our study suggests that CP and PDAC probably do not share genetic susceptibility, at least in terms of high frequency variants., (© 2017 UICC.)

Published
2018
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