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@ARTICLE{Amitay:154276,
      author       = {E. Amitay$^*$ and P. R. Carr$^*$ and L. Jansen$^*$ and W.
                      Roth and E. Alwers$^*$ and E. Herpel and M. Kloor and H.
                      Bläker and J. Chang-Claude$^*$ and H. Brenner$^*$ and M.
                      Hoffmeister$^*$},
      title        = {{S}moking, alcohol consumption and colorectal cancer risk
                      by molecular pathological subtypes and pathways.},
      journal      = {British journal of cancer},
      volume       = {122},
      number       = {11},
      issn         = {1532-1827},
      address      = {Edinburgh},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2020-00703},
      pages        = {1604-1610},
      year         = {2020},
      note         = {2020 May;122(11):1604-1610#EA:C070#LA:C070#},
      abstract     = {Smoking and alcohol increase risk for colorectal
                      malignancies. However, colorectal cancer (CRC) is a
                      heterogenic disease and associations with the molecular
                      pathological pathways are unclear.This population-based
                      case-control study includes 2444 cases with first-diagnosis
                      CRC and 2475 controls. Tumour tissue was analysed for MSI
                      (microsatellite instability), CIMP (CpG island methylator
                      phenotype), BRAF (B-Raf proto-oncogene serine/threonine
                      kinase gene) and KRAS (Kirsten rat sarcoma viral oncogene
                      homologue gene) mutations. Odds ratios (ORs) and $95\%$
                      confidence intervals $(95\%$ CIs) were estimated for
                      associations between alcohol and smoking and CRC molecular
                      subtypes and pathways.Current smoking showed higher ORs for
                      MSI-high (OR = 2.79, $95\%$ CI: 1.86-4.18) compared to
                      MSS (OR = 1.41, 1.14-1.75, p-heterogeneity
                      (p-het) = 0.001), BRAF-mutated (mut) (OR = 2.40,
                      1.41-4.07) compared to BRAF-wild type (wt) (OR = 1.52,
                      1.24-1.88, p-het = 0.074), KRAS-wt (OR = 1.70,
                      1.36-2.13) compared to KRAS-mut (OR = 1.26, 0.95-1.68,
                      p-het = 0.039) and CIMP-high (OR = 2.01, 1.40-2.88)
                      compared to CIMP-low/negative CRC (OR = 1.50, 1.22-1.85,
                      p-het=0.101). Current smoking seemed more strongly
                      associated with sessile serrated pathway
                      (CIMP-high + BRAF-mut; OR = 2.39, 1.27-4.52) than
                      with traditional pathway CRC
                      (MSS + CIMP-low/negative + BRAF-wt; OR = 1.50,
                      1.16-1.94) and no association was observed with alternate
                      pathway CRC (MSS + CIMP-low/negative + KRAS-wt;
                      OR = 1.08, 0.77-1.43). No heterogeneity was observed in
                      alcohol consumption association by molecular subtypes.In
                      this large case-control study, smoking was more strongly
                      associated with MSI-high and KRAS-wt CRC and with cases
                      showing features of the sessile serrated pathway.
                      Association patterns were less clear for alcohol
                      consumption.},
      cin          = {C070 / C120 / HD01 / C020},
      ddc          = {610},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
                      I:(DE-He78)HD01-20160331 / I:(DE-He78)C020-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32225169},
      doi          = {10.1038/s41416-020-0803-0},
      url          = {https://inrepo02.dkfz.de/record/154276},
}