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@ARTICLE{Gregg:181396,
      author       = {J. R. Gregg and J. Kim and C. Logothetis and S. Hanash and
                      X. Zhang and G. Manyam and K. Muir and G. G. Giles and J. L.
                      Stanford and S. I. Berndt and M. Kogevinas and H.
                      Brenner$^*$ and R. A. Eeles and P. Wei and C. R. Daniel},
      collaboration = {U. C. Group and P. Consortium},
      title        = {{C}offee {I}ntake, {C}affeine {M}etabolism {G}enotype, and
                      {S}urvival {A}mong {M}en with {P}rostate {C}ancer.},
      journal      = {European urology oncology},
      volume       = {6},
      number       = {3},
      issn         = {2588-9311},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2022-01964},
      pages        = {282-288},
      year         = {2023},
      note         = {2023 Jun;6(3):282-288},
      abstract     = {Coffee intake may lower prostate cancer risk and
                      progression, but postdiagnosis outcomes by caffeine
                      metabolism genotype are not well characterized.To evaluate
                      associations between coffee intake, caffeine metabolism
                      genotype, and survival in a large, multicenter study of men
                      with prostate cancer.Data from The PRACTICAL Consortium
                      database for 5727 men with prostate cancer from seven US,
                      Australian, and European studies were included. The cases
                      included had data available for the CYP1A2 -163C>A rs762551
                      single-nucleotide variant associated with caffeine
                      metabolism, coffee intake, and >6 mo of
                      follow-up.Multivariable-adjusted Cox proportional hazards
                      models across pooled patient-level data were used to compare
                      the effect of coffee intake (categorized as low [reference],
                      high, or none/very low) in relation to overall survival (OS)
                      and prostate cancer-specific survival (PCSS), with
                      stratified analyses conducted by clinical disease risk and
                      genotype.High coffee intake appeared to be associated with
                      longer PCSS (hazard ratio [HR] 0.85, $95\%$ confidence
                      interval [CI] 0.68-1.08; p = 0.18) and OS (HR 0.90, $95\%$
                      CI 0.77-1.07; p = 0.24), although results were not
                      statistically significant. In the group with clinically
                      localized disease, high coffee intake was associated with
                      longer PCSS (HR 0.66, $95\%$ CI 0.44-0.98; p = 0.040), with
                      comparable results for the group with advanced disease (HR
                      0.92, $95\%$ CI 0.69-1.23; p = 0.6). High coffee intake was
                      associated with longer PCSS among men with the CYP1A2 AA (HR
                      0.67, $95\%$ CI 0.49-0.93; p = 0.017) but not the AC/CC
                      genotype (p = 0.8); an interaction was detected (p = 0.042).
                      No associations with OS were observed in subgroup analyses
                      (p > 0.05). Limitations include the nominal statistical
                      significance and residual confounding.Coffee intake was
                      associated with longer PCSS among men with a CYP1A2 -163AA
                      (*1F/*1F) genotype, a finding that will require further
                      replication.It is likely that coffee intake is associated
                      with longer prostate cancer-specific survival in certain
                      groups, but more research is needed to fully understand
                      which men may benefit and why.},
      keywords     = {Caffeine (Other) / Coffee (Other) / Genetic variation
                      (Other) / Mortality (Other) / Prostatic neoplasms (Other)},
      cin          = {C070 / C120 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
                      I:(DE-He78)HD01-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35995710},
      doi          = {10.1016/j.euo.2022.07.008},
      url          = {https://inrepo02.dkfz.de/record/181396},
}