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@ARTICLE{Li:154479,
      author       = {C. Li and S. Stoma and L. A. Lotta and S. Warner and E.
                      Albrecht and A. Allione and P. P. Arp and L. Broer and J. L.
                      Buxton and A. Da Silva Couto Alves and J. Deelen and I. O.
                      Fedko and S. D. Gordon and T. Jiang and R. Karlsson and N.
                      Kerrison and T. K. Loe and M. Mangino and Y. Milaneschi and
                      B. Miraglio and N. Pervjakova and A. Russo and I. Surakka
                      and A. van der Spek and J. E. Verhoeven and N. Amin and M.
                      Beekman and A. I. Blakemore and F. Canzian$^*$ and S. E.
                      Hamby and J.-J. Hottenga and P. D. Jones and P. Jousilahti
                      and R. Mägi and S. E. Medland and G. W. Montgomery and D.
                      R. Nyholt and M. Perola and K. H. Pietiläinen and V.
                      Salomaa and E. Sillanpää and H. E. Suchiman and D. van
                      Heemst and G. Willemsen and A. Agudo and H. Boeing and D. I.
                      Boomsma and M.-D. Chirlaque and G. Fagherazzi and P. Ferrari
                      and P. Franks and C. Gieger and J. G. Eriksson and M. Gunter
                      and S. Hägg and I. Hovatta and L. Imaz and J. Kaprio and R.
                      Kaaks$^*$ and T. Key and V. Krogh and N. G. Martin and O.
                      Melander and A. Metspalu and C. Moreno and N. C.
                      Onland-Moret and P. Nilsson and K. K. Ong and K. Overvad and
                      D. Palli and S. Panico and N. L. Pedersen and B. W. J. H.
                      Penninx and J. R. Quirós and M. R. Jarvelin and M.
                      Rodríguez-Barranco and R. A. Scott and G. Severi and P. E.
                      Slagboom and T. D. Spector and A. Tjonneland and A.
                      Trichopoulou and R. Tumino and A. G. Uitterlinden and Y. T.
                      van der Schouw and C. M. van Duijn and E. Weiderpass and E.
                      L. Denchi and G. Matullo and A. S. Butterworth and J. Danesh
                      and N. J. Samani and N. J. Wareham and C. P. Nelson and C.
                      Langenberg and V. Codd},
      title        = {{G}enome-wide {A}ssociation {A}nalysis in {H}umans {L}inks
                      {N}ucleotide {M}etabolism to {L}eukocyte {T}elomere
                      {L}ength.},
      journal      = {The American journal of human genetics},
      volume       = {106},
      number       = {3},
      issn         = {0002-9297},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2020-00801},
      pages        = {389 - 404},
      year         = {2020},
      abstract     = {Leukocyte telomere length (LTL) is a heritable biomarker of
                      genomic aging. In this study, we perform a genome-wide
                      meta-analysis of LTL by pooling densely genotyped and
                      imputed association results across large-scale
                      European-descent studies including up to 78,592 individuals.
                      We identify 49 genomic regions at a false dicovery rate
                      (FDR) < 0.05 threshold and prioritize genes at 31, with five
                      highlighting nucleotide metabolism as an important regulator
                      of LTL. We report six genome-wide significant loci in or
                      near SENP7, MOB1B, CARMIL1, PRRC2A, TERF2, and RFWD3, and
                      our results support recently identified PARP1, POT1, ATM,
                      and MPHOSPH6 loci. Phenome-wide analyses in >350,000 UK
                      Biobank participants suggest that genetically shorter
                      telomere length increases the risk of hypothyroidism and
                      decreases the risk of thyroid cancer, lymphoma, and a range
                      of proliferative conditions. Our results replicate
                      previously reported associations with increased risk of
                      coronary artery disease and lower risk for multiple cancer
                      types. Our findings substantially expand current knowledge
                      on genes that regulate LTL and their impact on human health
                      and disease.},
      cin          = {C055 / C020},
      ddc          = {570},
      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:32109421},
      pmc          = {pmc:PMC7058826},
      doi          = {10.1016/j.ajhg.2020.02.006},
      url          = {https://inrepo02.dkfz.de/record/154479},
}