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@ARTICLE{Dahmen:837944,
      author       = {Dahmen, Volker and Schmitz, Sabine and Kriehuber, Ralf},
      title        = {{I}nduction of the chromosomal translocation t(14;18) by
                      targeting the {BCL}-2 locus with specific binding
                      {I}-125-labeled triplex-forming oligonucleotides},
      journal      = {Mutation research / Genetic toxicology and environmental
                      mutagenesis},
      volume       = {823},
      issn         = {1383-5718},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {FZJ-2017-06705},
      pages        = {58 - 64},
      year         = {2017},
      abstract     = {Triplex-Forming oligonucleotides (TFO) bind
                      sequence-specific to the DNA double helix in-vitro and
                      in-vivo andare a promising tool to manipulate genes or gene
                      regulatory elements. TFO as a carrier molecule for
                      short-rangeparticle emitter such as Auger-Electron-Emitters
                      (AEE) bear the potential to introduce radiation-induced
                      sitespecificcomplex DNA lesions, which are known to induce
                      chromosomal translocations. We studied gene
                      expression,translocation frequency and protein expression in
                      SCL-II cells after transfection with the AEE Iodine-125
                      (I-125) labeled TFO-BCL2 targeting the human BCL2 gene. The
                      TFO-BCL2 binds to the BCL2 gene in closeproximity to a known
                      major-breakage-region (mbr). SCL-II cells were transfected
                      with I-125 labeled TFO andstored for decay accumulation.
                      Monitoring of BCL2 translocations was done with the
                      Fluorescence-In-Situ-Hybridization (FISH) method. The
                      utilized FISH probes were designed to detect a t(14;18)
                      translocation of theBCL2 gene, which is a common
                      translocation leading to an overexpression of BCL2 protein.
                      Analysis of BCL2gene expression levels was done via
                      quantitative Real-Time PCR. Verification of gene expression
                      on the proteinlevel was analyzed by Western blotting. The
                      relative gene expression of BCL2 in I-125-TFO-BCL2
                      transfectedcells showed a significant up-regulation when
                      compared to controls. Analysis of the BCL2 t(14;18)
                      translocationfrequency revealed a significant 1.8- to 2-fold
                      increase when compared to control cells. This 2-fold
                      increase wasnot reflected on the protein level. We conclude
                      that I-125 decays within the BCL2 gene facilitate the
                      t(14;18)chromosomal translocation in the SCL-II cells and
                      that the increased frequency contributes to the
                      observedoverall enhanced BCL2 gene expression.},
      cin          = {S-US},
      ddc          = {570},
      cid          = {I:(DE-Juel1)S-US-20090406},
      pnm          = {899 - ohne Topic (POF3-899)},
      pid          = {G:(DE-HGF)POF3-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28985947},
      UT           = {WOS:000413615100006},
      doi          = {10.1016/j.mrgentox.2017.09.002},
      url          = {https://juser.fz-juelich.de/record/837944},
}