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@ARTICLE{Drew:290551,
      author       = {D. A. Drew and A. E. Kim and Y. Lin and C. Qu and J.
                      Morrison and J. P. Lewinger and E. Kawaguchi and J. Wang and
                      Y. Fu and N. Zemlianskaia and V. Díez-Obrero and S. A. Bien
                      and N. Dimou and D. Albanes and J. W. Baurley and A. H. Wu
                      and D. D. Buchanan and J. D. Potter and R. L. Prentice and
                      S. Harlid and V. Arndt$^*$ and E. L. Barry and S. I. Berndt
                      and E. Bouras and H. Brenner$^*$ and A. Budiarto and A.
                      Burnett-Hartman and P. T. Campbell and R. Carreras-Torres
                      and G. Casey and J. Chang-Claude$^*$ and D. V. Conti and M.
                      A. M. Devall and J. C. Figueiredo 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 A. Kundaje and L. Le Marchand and L. Li and
                      B. M. Lynch and N. Murphy and R. Nassir and P. A. Newcomb
                      and C. C. Newton 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. J. Pellatt and A. R. Peoples 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 M.
                      C. Stern and Y.-R. Su and D. C. Thomas and Y. Tian and K. K.
                      Tsilidis and C. M. Ulrich and C. Y. Um and F. J. B. van
                      Duijnhoven and B. Van Guelpen and E. White and L. Hsu and V.
                      Moreno and U. Peters and A. T. Chan and W. J. Gauderman},
      title        = {{T}wo genome-wide interaction loci modify the association
                      of nonsteroidal anti-inflammatory drugs with colorectal
                      cancer.},
      journal      = {Science advances},
      volume       = {10},
      number       = {22},
      issn         = {2375-2548},
      address      = {Washington, DC [u.a.]},
      publisher    = {Assoc.},
      reportid     = {DKFZ-2024-01155},
      pages        = {eadk3121},
      year         = {2024},
      abstract     = {Regular, long-term aspirin use may act synergistically with
                      genetic variants, particularly those in mechanistically
                      relevant pathways, to confer a protective effect on
                      colorectal cancer (CRC) risk. We leveraged pooled data from
                      52 clinical trial, cohort, and case-control studies that
                      included 30,806 CRC cases and 41,861 controls of European
                      ancestry to conduct a genome-wide interaction scan between
                      regular aspirin/nonsteroidal anti-inflammatory drug (NSAID)
                      use and imputed genetic variants. After adjusting for
                      multiple comparisons, we identified statistically
                      significant interactions between regular aspirin/NSAID use
                      and variants in 6q24.1 (top hit rs72833769), which has
                      evidence of influencing expression of TBC1D7 (a subunit of
                      the TSC1-TSC2 complex, a key regulator of MTOR activity),
                      and variants in 5p13.1 (top hit rs350047), which is
                      associated with expression of PTGER4 (codes a cell surface
                      receptor directly involved in the mode of action of
                      aspirin). Genetic variants with functional impact may
                      modulate the chemopreventive effect of regular aspirin use,
                      and our study identifies putative previously unidentified
                      targets for additional mechanistic interrogation.},
      keywords     = {Humans / Colorectal Neoplasms: genetics / Colorectal
                      Neoplasms: drug therapy / Anti-Inflammatory Agents,
                      Non-Steroidal: pharmacology / Genome-Wide Association Study
                      / Polymorphism, Single Nucleotide / Aspirin: pharmacology /
                      Receptors, Prostaglandin E, EP4 Subtype: genetics /
                      Receptors, Prostaglandin E, EP4 Subtype: metabolism / Male /
                      Genetic Predisposition to Disease / Female / Case-Control
                      Studies / Middle Aged / Genetic Loci / Aged /
                      Anti-Inflammatory Agents, Non-Steroidal (NLM Chemicals) /
                      Aspirin (NLM Chemicals) / Receptors, Prostaglandin E, EP4
                      Subtype (NLM Chemicals) / PTGER4 protein, human (NLM
                      Chemicals)},
      cin          = {C070 / C120 / HD01 / C020 / C071},
      ddc          = {500},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
                      I:(DE-He78)HD01-20160331 / I:(DE-He78)C020-20160331 /
                      I:(DE-He78)C071-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38809988},
      pmc          = {pmc:PMC11135391},
      doi          = {10.1126/sciadv.adk3121},
      url          = {https://inrepo02.dkfz.de/record/290551},
}