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@ARTICLE{Schmeiser:128270,
      author       = {H. Schmeiser$^*$ and J. L. Nortier and R. Singh and G.
                      Gamboa da Costa and J. Sennesael and E. Cassuto-Viguier and
                      D. Ambrosetti and S. Rorive and A. Pozdzik and D. H.
                      Phillips and M. Stiborova and V. M. Arlt},
      title        = {{E}xceptionally long-term persistence of {DNA} adducts
                      formed by carcinogenic aristolochic acid {I} in renal tissue
                      from patients with aristolochic acid nephropathy.},
      journal      = {International journal of cancer},
      volume       = {135},
      number       = {2},
      issn         = {0020-7136},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2017-04287},
      pages        = {502-507},
      year         = {2014},
      abstract     = {Aristolochic acid (AA) causes aristolochic acid nephropathy
                      (AAN), first described in women in Belgium accidently
                      prescribed Aristolochia fangchi in a slimming treatment, and
                      also Balkan endemic nephropathy (BEN), through probable
                      dietary contamination with Aristolochia clematitis seeds.
                      Both nephropathies have a high risk of urothelial cancer,
                      with AA being the causative agent. In tissues of AAN and BEN
                      patients, a distinct DNA adduct,
                      7-(deoxyadenosin-N6-yl)-aristolactam I (dA-AAI), has been
                      detected. DNA adducts can be removed through DNA repair,
                      they can result in mutations through erroneous DNA
                      replication or they can cause cell death. The dA-AAI adduct
                      induces AT to TA transversions in the tumor-suppressor TP53
                      gene in experimental systems, matching TP53 mutations
                      observed in urothelial tumors from AAN cancer cases. Using
                      thin-layer chromatography 32P-postlabeling and mass
                      spectrometric analysis we report the detection of dA-AAI in
                      renal DNA from 11 Belgian AAN patients over 20 years after
                      exposure to AA had ceased. Our results showed that dA-AAI is
                      an established biomarker of AA exposure, and that this
                      biomarker can be demonstrated to be persistent decades after
                      a distinct AA exposure. Further, the persistence of dA-AAI
                      adducts appears to be a critical determinant for the AA
                      mutational fingerprint frequently found in oncogenes and
                      tumor suppressor genes recently identified by whole genome
                      sequencing of AA-associated urothelial tumors. The potential
                      for exposure to AA worldwide is high; the unprecedented
                      long-term persistence of dA-AAI provides a useful long-term
                      biomarker of exposure and attests to the role of AA in human
                      urothelial malignancy.},
      keywords     = {Aristolochic Acids (NLM Chemicals) / Biomarkers (NLM
                      Chemicals) / DNA Adducts (NLM Chemicals) / Mutagens (NLM
                      Chemicals) / aristolochic acid I (NLM Chemicals)},
      cin          = {C016 / E030},
      ddc          = {610},
      cid          = {I:(DE-He78)C016-20160331 / I:(DE-He78)E030-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24921086},
      url          = {https://inrepo02.dkfz.de/record/128270},
}