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dc.contributor.authorCampa, Daniele
dc.contributor.authorPastore, Manuela
dc.contributor.authorCapurso, Gabriele
dc.contributor.authorHackert, Thilo
dc.contributor.authorDi Leo, Milena
dc.contributor.authorIzbicki, Jakob R
dc.contributor.authorKhaw, Kay-Tee
dc.contributor.authorGioffreda, Domenica
dc.contributor.authorKupcinskas, Juozas
dc.contributor.authorPasquali, Claudio
dc.contributor.authorMacinga, Peter
dc.contributor.authorKaaks, Rudolf
dc.contributor.authorStigliano, Serena
dc.contributor.authorPeeters, Petra H
dc.contributor.authorKey, Timothy J
dc.contributor.authorTalar-Wojnarowska, Renata
dc.contributor.authorVodicka, Pavel
dc.contributor.authorValente, Roberto
dc.contributor.authorVashist, Yogesh K
dc.contributor.authorSalvia, Roberto
dc.contributor.authorPapaconstantinou, Ioannis
dc.contributor.authorShimizu, Yasuhiro
dc.contributor.authorValsuani, Chiara
dc.contributor.authorZambon, Carlo Federico
dc.contributor.authorGazouli, Maria
dc.contributor.authorValantiene, Irena
dc.contributor.authorNiesen, Willem
dc.contributor.authorMohelnikova-Duchonova, Beatrice
dc.contributor.authorHara, Kazuo
dc.contributor.authorSoucek, Pavel
dc.contributor.authorMalecka-Panas, Ewa
dc.contributor.authorBueno-de-Mesquita, H B As
dc.contributor.authorJohnson, Theron
dc.contributor.authorBrenner, Herman
dc.contributor.authorTavano, Francesca
dc.contributor.authorFogar, Paola
dc.contributor.authorIto, Hidemi
dc.contributor.authorSperti, Cosimo
dc.contributor.authorButterbach, Katja
dc.contributor.authorLatiano, Anna
dc.contributor.authorAndriulli, Angelo
dc.contributor.authorCavestro, Giulia Martina
dc.contributor.authorBusch, Olivier R C
dc.contributor.authorDijk, Frederike
dc.contributor.authorGreenhalf, William
dc.contributor.authorMatsuo, Keitaro
dc.contributor.authorLombardo, Carlo
dc.contributor.authorStrobel, Oliver
dc.contributor.authorKönig, Anna-Katharina
dc.contributor.authorCuk, Katarina
dc.contributor.authorStrothmann, Hendrik
dc.contributor.authorKatzke, Verena
dc.contributor.authorCantore, Maurizio
dc.contributor.authorMambrini, Andrea
dc.contributor.authorOliverius, Martin
dc.contributor.authorPezzilli, Raffaele
dc.contributor.authorLandi, Stefano
dc.contributor.authorCanzian, Federico
dc.date.accessioned2018-01-10T07:37:59Z
dc.date.available2018-01-10T07:37:59Z
dc.date.issued2018-01-15
dc.identifier.citationDo pancreatic cancer and chronic pancreatitis share the same genetic risk factors? A PANcreatic Disease ReseArch (PANDoRA) consortium investigation. 2018, 142 (2):290-296 Int. J. Canceren
dc.identifier.issn1097-0215
dc.identifier.pmid28913878
dc.identifier.doi10.1002/ijc.31047
dc.identifier.urihttp://hdl.handle.net/10029/621113
dc.description.abstractPancreatic 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 (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 = 1.10 × 10-6 ) and MORC4-rs 12837024 (ORhomozygous  = 2.07 (1.55-2.77, ptrend  = 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.
dc.language.isoenen
dc.rightsArchived with thanks to International journal of canceren
dc.subject.meshAdenocarcinoma
dc.subject.meshAdult
dc.subject.meshAged
dc.subject.meshBiomarkers, Tumor
dc.subject.meshCarcinoma, Pancreatic Ductal
dc.subject.meshCase-Control Studies
dc.subject.meshFemale
dc.subject.meshFollow-Up Studies
dc.subject.meshHumans
dc.subject.meshMale
dc.subject.meshMiddle Aged
dc.subject.meshNuclear Proteins
dc.subject.meshPancreatic Neoplasms
dc.subject.meshPancreatitis, Chronic
dc.subject.meshPolymorphism, Single Nucleotide
dc.subject.meshPrognosis
dc.subject.meshRetrospective Studies
dc.subject.meshRisk Factors
dc.subject.meshTrypsin
dc.subject.meshTrypsinogen
dc.titleDo pancreatic cancer and chronic pancreatitis share the same genetic risk factors? A PANcreatic Disease ReseArch (PANDoRA) consortium investigation.en
dc.typeArticleen
dc.identifier.journalInt J Cancer 2018, 142(2):290-6en
html.description.abstractPancreatic 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 (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 = 1.10 × 10-6 ) and MORC4-rs 12837024 (ORhomozygous  = 2.07 (1.55-2.77, ptrend  = 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.


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