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@ARTICLE{Wang:157054,
      author       = {X. Wang and Y.-R. Su and P. S. Petersen and S. Bien and S.
                      L. Schmit and D. A. Drew and D. Albanes and S. I. Berndt and
                      H. Brenner$^*$ and P. T. Campbell and G. Casey and J.
                      Chang-Claude$^*$ and S. Gallinger and S. B. Gruber and R. W.
                      Haile and T. A. Harrison and M. Hoffmeister$^*$ and E. J.
                      Jacobs and M. A. Jenkins and A. D. Joshi and L. Li and Y.
                      Lin and N. M. Lindor and L. Le Marchand and V. Martín and
                      R. L. Milne and R. Maclnnis and V. Moreno and H. Nan and P.
                      A. Newcomb and J. D. Potter and G. Rennert and H. S. Rennert
                      and M. L. Slattery and S. N. Thibodeau and S. J. Weinstein
                      and M. O. Woods and A. T. Chan and E. White and L. Hsu and
                      U. Peters},
      title        = {{E}xploratory genome-wide interaction analysis of
                      non-steroidal anti-inflammatory drugs and predicted gene
                      expression on colorectal cancer risk.},
      journal      = {Cancer epidemiology, biomarkers $\&$ prevention},
      volume       = {29},
      number       = {9},
      issn         = {1538-7755},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2020-01345},
      pages        = {1800-1808},
      year         = {2020},
      note         = {2020 Sep;29(9):1800-1808},
      abstract     = {Regular use of non-steroidal anti-inflammatory drugs
                      (NSAIDs) is associated with lower risk of colorectal cancer
                      (CRC). Genome-wide interaction analysis on single variants
                      (G×E) has identified several SNPs that may interact with
                      NSAIDs to confer CRC risk, but variations in gene expression
                      levels may also modify the effect of NSAID use. Therefore,
                      we tested interactions between NSAID use and predicted gene
                      expression levels in relation to CRC risk.Genetically
                      predicted gene expressions were tested for interaction with
                      NSAID use on CRC risk among 19,258 CRC cases and 18,597
                      controls from 21 observational studies. A Mixed Score Test
                      for Interactions (MiSTi) approach was used to jointly assess
                      G×E effects which are modeled via fixed interaction effects
                      of the weighted burden within each gene sets (burden) and
                      residual G×E effects (variance). A false discovery rate
                      (FDR) at 0.2 was applied to correct for multiple
                      testing.Among the 4,840 genes tested, genetically predicted
                      expression levels of four genes modified the effect of any
                      NSAID use on CRC risk, including DPP10 (P-G×E=1.96×10-4),
                      KRT16 (P-G×E=2.3×10-4), CD14 (P-G×E=9.38×10-4), and
                      CYP27A1 (P-G×E=1.44×10-3). There was a significant
                      interaction between expression level of RP11-89N17 and
                      regular use of aspirin only on CRC risk (P-G×E=3.23×10-5).
                      No interactions were observed between predicted gene
                      expression and non-aspirin NSAID use at FDR<0.2.By
                      incorporating functional information, we discovered several
                      novel genes that interacted with NSAID use.These findings
                      provide preliminary support that could help understand the
                      chemopreventive mechanisms of NSAIDs on CRC.},
      cin          = {C070 / C020 / C120 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)C020-20160331 /
                      I:(DE-He78)C120-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32651213},
      doi          = {10.1158/1055-9965.EPI-19-1018},
      url          = {https://inrepo02.dkfz.de/record/157054},
}