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@ARTICLE{Zimmer:147295,
      author       = {P. Zimmer$^*$ and M. E. Schmidt$^*$ and M. T. Prentzell$^*$
                      and B. Berdel$^*$ and J. Wiskemann and K. H. Kellner and J.
                      Debus and C. Ulrich and C. A. Opitz$^*$ and K.
                      Steindorf$^*$},
      title        = {{R}esistance {E}xercise {R}educes {K}ynurenine {P}athway
                      {M}etabolites in {B}reast {C}ancer {P}atients {U}ndergoing
                      {R}adiotherapy.},
      journal      = {Frontiers in oncology},
      volume       = {9},
      issn         = {2234-943X},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DKFZ-2019-02416},
      pages        = {962},
      year         = {2019},
      abstract     = {Purpose: Evidence from preclinical studies and trials in
                      healthy volunteers suggests that exercise may modulate the
                      levels of tryptophan (TRP) metabolites along the kynurenine
                      (KYN) pathway. As KYN and downstream KYN metabolites are
                      known to promote cancer progression by inhibiting anti-tumor
                      immune responses and by promoting the motility of cancer
                      cells, we investigated if resistance exercise can also
                      control the levels of KYN pathway metabolites in breast
                      cancer patients undergoing radiotherapy (NCT01468766).
                      Patients and Methods: Chemotherapy-naïve breast cancer
                      patients (n = 96) were either randomized to an
                      exercise/intervention group (IG) or a control group (CG).
                      The IG participated in a 12-week supervised progressive
                      resistance exercise program twice a week, whereas the CG
                      received a supervised relaxation program. Serum levels of
                      TRP and KYN as well as urine levels of kynurenic acid (KYNA)
                      and neurotoxic quinolinic acid (QUINA) were assessed before
                      (t0), after radiotherapy, and mid-term of the exercise
                      intervention (t1) and after the exercise intervention (t2).
                      Additionally, 24 healthy women (HIG) participated in the
                      exercise program to investigate potential differences in its
                      effects on KYN metabolites in comparison to the breast
                      cancer patients. Results: At baseline (t0) the breast cancer
                      patients showed a significantly elevated serum KYN/TRP ratio
                      and urine QUINA/KYNA ratio, as well as increased urine QUINA
                      levels in comparison to the healthy women. In response to
                      exercise the healthy women and the breast cancer patients
                      differed significantly in the levels of urine QUINA and the
                      QUINA/KYNA ratio. Most importantly, serum KYN levels and the
                      KYN/TRP ratio were significantly reduced in exercising
                      patients (IG) compared to non-exercising patients (CG) both
                      at t1 and t2. Conclusion: Resistance exercise may represent
                      a potent non-pharmacological avenue to counteract an
                      activation of the KYN pathway in breast cancer patients
                      undergoing radiotherapy.},
      cin          = {C110 / B350 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)C110-20160331 / I:(DE-He78)B350-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31612110},
      pmc          = {pmc:PMC6773833},
      doi          = {10.3389/fonc.2019.00962},
      url          = {https://inrepo02.dkfz.de/record/147295},
}