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@ARTICLE{CarrerasTorres:186491,
      author       = {R. Carreras-Torres and A. E. Kim and Y. Lin and V.
                      Díez-Obrero and S. A. Bien and C. Qu and J. Wang and N.
                      Dimou and E. K. Aglago and D. Albanes and V. Arndt$^*$ and
                      J. W. Baurley and S. I. Berndt and S. Bézieau and D. T.
                      Bishop and E. Bouras and H. Brenner$^*$ and A. Budiarto and
                      P. T. Campbell and G. Casey and A. T. Chan and J.
                      Chang-Claude$^*$ and X. Chen$^*$ and D. V. Conti and C. H.
                      Dampier and M. A. Devall and D. A. Drew and J. C. Figueiredo
                      and S. Gallinger and G. G. Giles and S. B. Gruber and A.
                      Gsur and M. J. Gunter and T. A. Harrison and A. Hidaka and
                      M. Hoffmeister$^*$ and J. R. Huyghe and M. A. Jenkins and K.
                      M. Jordahl and E. Kawaguchi and T. O. Keku and A. Kundaje
                      and L. Le Marchand and J. P. Lewinger and L. Li and B.
                      Mahesworo and J. L. Morrison and N. Murphy and H. Nan and R.
                      Nassir and P. A. Newcomb and M. Obón-Santacana and S. Ogino
                      and J. Ose and R. K. Pai and J. R. Palmer and N.
                      Papadimitriou and B. Pardamean and A. R. Peoples and P. D.
                      P. Pharoah and E. A. Platz and G. Rennert and E.
                      Ruiz-Narvaez and L. C. Sakoda and P. C. Scacheri and S. L.
                      Schmit and R. E. Schoen and A. Shcherbina and M. L. Slattery
                      and M. C. Stern and Y.-R. Su and C. M. Tangen and D. C.
                      Thomas and Y. Tian and K. K. Tsilidis and C. M. Ulrich and
                      F. J. B. van Duijnhoven and B. Van Guelpen and K.
                      Visvanathan and P. Vodicka and T. W. Cenggoro and S. J.
                      Weinstein and E. White and A. Wolk and M. O. Woods and L.
                      Hsu and U. Peters and V. Moreno and W. J. Gauderman},
      title        = {{G}enome-wide interaction study with smoking for colorectal
                      cancer risk identifies novel genetic loci related to tumor
                      suppression, inflammation and immune response.},
      journal      = {Cancer epidemiology, biomarkers $\&$ prevention},
      volume       = {32},
      number       = {3},
      issn         = {1055-9965},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2022-03212},
      pages        = {315-328},
      year         = {2023},
      note         = {2023 Mar 6;32(3):315-328},
      abstract     = {Tobacco smoking is an established risk factor for
                      colorectal cancer (CRC). However, genetically-defined
                      population subgroups may have increased susceptibility to
                      smoking-related effects on CRC.A genome-wide interaction
                      scan was performed including 33,756 CRC cases and 44,346
                      controls from three genetic consortia.Evidence of an
                      interaction was observed between smoking status (ever vs
                      never smokers) and a locus on 3p12.1 (rs9880919,
                      p=4.58x10-8), with higher associated risk in subjects
                      carrying the GG genotype (OR 1.25, $95\%CI$ 1.20-1.30)
                      compared with the other genotypes (OR <1.17 for GA and AA).
                      Among ever smokers, we observed interactions between smoking
                      intensity (increase in 10 cigarettes smoked per day) and two
                      loci on 6p21.33 (rs4151657, p=1.72x10-8) and 8q24.23
                      (rs7005722, p=2.88x10-8). Subjects carrying the rs4151657 TT
                      genotype showed higher risk (OR 1.12, $95\%CI$ 1.09-1.16)
                      compared with the other genotypes (OR <1.06 for TC and CC).
                      Similarly, higher risk was observed among subjects carrying
                      the rs7005722 AA genotype (OR 1.17, $95\%CI$ 1.07-1.28)
                      compared with the other genotypes (OR <1.13 for AC and CC).
                      Functional annotation revealed that SNPs in 3p12.1 and
                      6p21.33 loci were located in regulatory regions, and were
                      associated with expression levels of nearby genes. Genetic
                      models predicting gene expression revealed that smoking
                      parameters were associated with lower CRC risk with higher
                      expression levels of CADM2 (3p12.1) and ATF6B (6p21.33).Our
                      study identified novel genetic loci that may modulate the
                      risk for CRC of smoking status and intensity, linked to
                      tumor suppression and immune response.These findings can
                      guide potential prevention treatments.},
      cin          = {C071 / C070 / C020},
      ddc          = {610},
      cid          = {I:(DE-He78)C071-20160331 / I:(DE-He78)C070-20160331 /
                      I:(DE-He78)C020-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36576985},
      doi          = {10.1158/1055-9965.EPI-22-0763},
      url          = {https://inrepo02.dkfz.de/record/186491},
}