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@ARTICLE{Herzog:289070,
      author       = {C. Herzog and A. Jones and I. Evans and J. Raut$^*$ and M.
                      Zikan and D. Cibula and A. Wong and H. Brenner$^*$ and R. C.
                      Richmond and M. Widschwendter},
      title        = {{C}igarette smoking and e-cigarette use induce shared {DNA}
                      methylation changes linked to carcinogenesis.},
      journal      = {Cancer research},
      volume       = {84},
      number       = {11},
      issn         = {0099-7013},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2024-00571},
      pages        = {1898-1914},
      year         = {2024},
      note         = {2024 Jun 4;84(11):1898-1914},
      abstract     = {Tobacco use is a major modifiable risk factor for adverse
                      health outcomes, including cancer, and elicits profound
                      epigenetic changes thought to be associated with long-term
                      cancer risk. While electronic cigarettes (e-cigarettes) have
                      been advocated as harm reduction alternatives to tobacco
                      products, recent studies have revealed potential detrimental
                      effects, highlighting the urgent need for further research
                      into the molecular and health impacts of e-cigarettes. Here,
                      we applied computational deconvolution methods to dissect
                      the cell- and tissue-specific epigenetic effects of tobacco
                      or e-cigarette use on DNA methylation (DNAme) in over 3,500
                      buccal/saliva, cervical, or blood samples, spanning
                      epithelial and immune cells at directly and indirectly
                      exposed sites. The 535 identified smoking-related DNAme loci
                      (CpGs) clustered into four functional groups, including
                      detoxification or growth signaling, based on cell type and
                      anatomical site. Loci hypermethylated in buccal epithelial
                      cells of smokers associated with NOTCH1/RUNX3/growth factor
                      receptor signaling also exhibited elevated methylation in
                      cancer tissue and progressing lung carcinoma in situ
                      lesions, and hypermethylation of these sites predicted lung
                      cancer development in buccal samples collected from smokers
                      up to 22 years prior to diagnosis, suggesting a potential
                      role in driving carcinogenesis. Alarmingly, these CpGs were
                      also hypermethylated in e-cigarette users with a limited
                      smoking history. This study sheds light on the cell
                      type-specific changes to the epigenetic landscape induced by
                      smoking-related products.},
      cin          = {C070 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38503267},
      doi          = {10.1158/0008-5472.CAN-23-2957},
      url          = {https://inrepo02.dkfz.de/record/289070},
}