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@ARTICLE{Campa:131718,
author = {D. Campa and M. Pastore$^*$ and G. Capurso and T. Hackert
and M. Di Leo and J. R. Izbicki and K.-T. Khaw and D.
Gioffreda and J. Kupcinskas and C. Pasquali and P. Macinga
and R. Kaaks$^*$ and S. Stigliano and P. H. Peeters and T.
J. Key and R. Talar-Wojnarowska and P. Vodicka and R.
Valente and Y. K. Vashist and R. Salvia and I.
Papaconstantinou and Y. Shimizu and C. Valsuani and C. F.
Zambon and M. Gazouli and I. Valantiene and W. Niesen and B.
Mohelnikova-Duchonova and K. Hara and P. Soucek and E.
Malecka-Panas and H. B. A. Bueno-de-Mesquita and T. S.
Johnson$^*$ and H. Brenner$^*$ and F. Tavano and P. Fogar
and H. Ito and C. Sperti and K. Butterbach$^*$ and A.
Latiano and A. Andriulli and G. M. Cavestro and O. R. C.
Busch and F. Dijk and W. Greenhalf and K. Matsuo and C.
Lombardo and O. Strobel and A.-K. König and K. Cuk$^*$ and
H. Strothmann and V. Katzke$^*$ and M. Cantore and A.
Mambrini and M. Oliverius and R. Pezzilli and S. Landi and
F. Canzian$^*$},
title = {{D}o pancreatic cancer and chronic pancreatitis share the
same genetic risk factors? {A} {PAN}creatic {D}isease
{R}ese{A}rch ({PAND}o{RA}) consortium investigation.},
journal = {International journal of cancer},
volume = {142},
number = {2},
issn = {0020-7136},
address = {Bognor Regis},
publisher = {Wiley-Liss},
reportid = {DKFZ-2018-00024},
pages = {290 - 296},
year = {2018},
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 (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.},
keywords = {Biomarkers, Tumor (NLM Chemicals) / MORC4 protein, human
(NLM Chemicals) / Nuclear Proteins (NLM Chemicals) / PRSS2
protein, human (NLM Chemicals) / Trypsinogen (NLM Chemicals)
/ PRSS1 protein, human (NLM Chemicals) / Trypsin (NLM
Chemicals)},
cin = {C055 / C020 / C070 / G110 / L101},
ddc = {610},
cid = {I:(DE-He78)C055-20160331 / I:(DE-He78)C020-20160331 /
I:(DE-He78)C070-20160331 / I:(DE-He78)G110-20160331 /
I:(DE-He78)L101-20160331},
pnm = {313 - Cancer risk factors and prevention (POF3-313)},
pid = {G:(DE-HGF)POF3-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:28913878},
doi = {10.1002/ijc.31047},
url = {https://inrepo02.dkfz.de/record/131718},
}