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@ARTICLE{Stewart:170152,
      author       = {K. L. Stewart and B. Gigic and C. Himbert and C. A. Warby
                      and J. Ose and T. Lin and P. Schrotz-King$^*$ and J. Boehm
                      and K. C. Jordan and J. Metos and M. Schneider and J. C.
                      Figueiredo and C. I. Li and D. Shibata and E. Siegel and A.
                      T. Toriola and S. Hardikar and C. M. Ulrich},
      title        = {{A}ssociation of {S}ugar {I}ntake with {I}nflammation- and
                      {A}ngiogenesis-{R}elated {B}iomarkers in {N}ewly {D}iagnosed
                      {C}olorectal {C}ancer {P}atients.},
      journal      = {Nutrition and cancer},
      volume       = {74},
      number       = {5},
      issn         = {1532-7914},
      address      = {New York, NY},
      publisher    = {Routledge, Taylor $\&$ Francis Group},
      reportid     = {DKFZ-2021-01782},
      pages        = {1636-1643},
      year         = {2022},
      note         = {2022;74(5):1636-1643},
      abstract     = {Evidence suggests a positive association between sugar
                      intake and colorectal cancer (CRC) outcomes. We sought to
                      investigate inflammation and angiogenesis as underlying
                      mechanisms behind increased sugar intake and worse CRC
                      outcomes. Pre-surgery serum samples were obtained from 191
                      patients diagnosed with primary invasive stage I-IV CRC.
                      Biomarkers of inflammation (CRP, SAA, IL-6, IL-8, MCP-1,
                      TNFα) and angiogenesis (VEGFA, VEGFD, sICAM-1 and sVCAM-1)
                      were analyzed (Meso-Scale-Discovery). Fructose, glucose,
                      sucrose, and total sugar intake (calories/day, $\%$ total
                      calories) were assessed by FFQ. Pearson's correlation and
                      multiple linear regression analyses were performed. Patients
                      were on average 64 years old, $64\%$ were male, the majority
                      was diagnosed with stage II-III $(58\%)$ cancers, and $67\%$
                      were either overweight or obese. Among normal-weight
                      individuals (BMI <25 kg/m2), we observed a significant
                      inverse association between VEGFD and any type of sugar
                      intake in cal/day (sucrose: p = 0.01, glucose and fructose:
                      p < 0.001) and MCP-1 and fructose intake (p = 0.05). The
                      magnitude of reduction in VEGF ranged between -1.24 for
                      sucrose to 4.49 for glucose intake, and -2.64 for fructose
                      intake for MCP-1 levels. Sugar intake was associated with
                      some inflammation or angiogenesis biomarkers, among CRC
                      patients; differences were observed by adiposity that
                      warrant further investigation.Supplemental data for this
                      article is available online at at
                      10.1080/01635581.2021.1957133.},
      cin          = {C120},
      ddc          = {610},
      cid          = {I:(DE-He78)C120-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34369225},
      doi          = {10.1080/01635581.2021.1957133},
      url          = {https://inrepo02.dkfz.de/record/170152},
}