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@ARTICLE{Campa:132793,
      author       = {D. Campa and M. Barrdahl$^*$ and A. Santoro and G. Severi
                      and L. Baglietto and H. Omichessan and R. Tumino and H. B.
                      A. Bueno-de-Mesquita and P. H. Peeters and E. Weiderpass and
                      M.-D. Chirlaque and M. Rodríguez-Barranco and A. Agudo and
                      M. Gunter and L. Dossus and V. Krogh and G. Matullo and A.
                      Trichopoulou and R. C. Travis and F. Canzian$^*$ and R.
                      Kaaks$^*$},
      title        = {{M}itochondrial {DNA} copy number variation, leukocyte
                      telomere length, and breast cancer risk in the {E}uropean
                      {P}rospective {I}nvestigation into {C}ancer and {N}utrition
                      ({EPIC}) study.},
      journal      = {Breast cancer research},
      volume       = {20},
      number       = {1},
      issn         = {1465-542X},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DKFZ-2018-00437},
      pages        = {29},
      year         = {2018},
      abstract     = {Leukocyte telomere length (LTL) and mitochondrial genome
                      (mtDNA) copy number and deletions have been proposed as risk
                      markers for various cancer types, including breast cancer
                      (BC).To gain a more comprehensive picture on how these
                      markers can modulate BC risk, alone or in conjunction, we
                      performed simultaneous measurements of LTL and mtDNA copy
                      number in up to 570 BC cases and 538 controls from the
                      European Prospective Investigation into Cancer and Nutrition
                      (EPIC) cohort. As a first step, we measured LTL and mtDNA
                      copy number in 96 individuals for which a blood sample had
                      been collected twice with an interval of 15 years.According
                      to the intraclass correlation (ICC), we found very good
                      stability over the time period for both measurements, with
                      ICCs of 0.63 for LTL and 0.60 for mtDNA copy number. In the
                      analysis of the entire study sample, we observed that longer
                      LTL was strongly associated with increased risk of BC (OR
                      2.71, $95\%$ CI 1.58-4.65, p = 3.07 × 10- 4 for highest
                      vs. lowest quartile; OR 3.20, $95\%$ CI 1.57-6.55, p = 1.41
                      × 10- 3 as a continuous variable). We did not find any
                      association between mtDNA copy number and BC risk; however,
                      when considering only the functional copies, we observed an
                      increased risk of developing estrogen receptor-positive BC
                      (OR 2.47, $95\%$ CI 1.05-5.80, p = 0.04 for highest vs.
                      lowest quartile).We observed a very good correlation between
                      the markers over a period of 15 years. We confirm a role of
                      LTL in BC carcinogenesis and suggest an effect of mtDNA copy
                      number on BC risk.},
      cin          = {C055 / C020},
      ddc          = {610},
      cid          = {I:(DE-He78)C055-20160331 / I:(DE-He78)C020-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29665866},
      pmc          = {pmc:PMC5905156},
      doi          = {10.1186/s13058-018-0955-5},
      url          = {https://inrepo02.dkfz.de/record/132793},
}