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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},
}