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@ARTICLE{Khl:140844,
      author       = {T. Kühl and S. Behrens$^*$ and A. Y. Jung$^*$ and N. Obi
                      and K. Thöne and M. Schmidt$^*$ and H. Becher and J.
                      Chang-Claude$^*$},
      title        = {{V}alidation of inflammatory genetic variants associated
                      with long-term cancer related fatigue in a large breast
                      cancer cohort.},
      journal      = {Brain, behavior and immunity},
      volume       = {73},
      issn         = {0889-1591},
      address      = {Orlando, Fla.},
      publisher    = {Academic Press},
      reportid     = {DKFZ-2018-01599},
      pages        = {252 - 260},
      year         = {2018},
      abstract     = {Studies to date have reported several associations between
                      single nucleotide polymorphisms (SNPs) and cancer related
                      fatigue (CRF), but have been limited by small sample sizes,
                      missing adjustment for relevant covariates or multiple
                      testing, as well as varying CRF definitions, i.e. time and
                      method of assessment. This study aimed to validate
                      previously reported associations using the largest
                      independent breast cancer sample to date and to evaluate
                      further functional cytokine variants in relation to total
                      CRF and all relevant CRF subdomains (physical, cognitive,
                      and affective CRF).45 candidate SNPs in inflammatory pathway
                      genes were selected based on previous reports (16 SNPs) or
                      regulatory function (29 SNPs). Breast cancer patients
                      recruited between 2002 and 2005 provided information on CRF
                      at first follow-up (FU1) (N = 1389) and second follow-up
                      (FU2) (N = 950), a median of 6.2 years and
                      11.7 years respectively after diagnosis. SNP associations
                      were assessed using linear regression models on CRF scores
                      separately for FU1 and FU2. Additionally, patients with
                      persistent fatigue (fatigued at both time-points) were
                      compared to those never fatigued using logistic regression
                      models (N = 684). All analyses were adjusted for
                      relevant covariates. Secondary analyses were conducted for
                      CRF subdomains.For total CRF none of the previously reported
                      associations were confirmed after correction for multiple
                      testing. The p-value distribution of all SNPs was not
                      different than the one expected by chance. Analyses of CRF
                      subdomains yielded a significant association between TNF-α
                      rs3093662 and persistent physical CRF (Odds Ratio
                      (OR) = 3.23, $95\%$ Confidence Interval
                      (CI) = 1.71-6.10, p = 0.0003).We were unable to
                      confirm previously reported findings, suggesting that
                      individual SNPs are unlikely to be of clinical utility.
                      Further investigations in well powered studies are
                      warranted, which consider genetic heterogeneity according to
                      subdomains of CRF.},
      cin          = {C020 / G210},
      ddc          = {150},
      cid          = {I:(DE-He78)C020-20160331 / I:(DE-He78)G210-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29763737},
      doi          = {10.1016/j.bbi.2018.05.009},
      url          = {https://inrepo02.dkfz.de/record/140844},
}