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@ARTICLE{Totis:359584,
      author       = {Totis, Cristina and Averbeck, Nicole B. and Jakob, Burkhard
                      and Schork, Maik and Volpi, Gaia and Hintze, Dennis F. and
                      Durante, Marco and Fournier, Claudia and Helm, Alexander},
      title        = {{I}nduction of {C}ytoplasmic ds{DNA} and c{GAS}-{STING}
                      {I}mmune {S}ignaling {A}fter {E}xposure of {B}reast {C}ancer
                      {C}ells to {X}-ray or {H}igh-{E}nergetic {C}arbon {I}ons},
      journal      = {Advances in radiation oncology},
      volume       = {10},
      number       = {6},
      issn         = {2452-1094},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {GSI-2025-00765},
      pages        = {101783},
      year         = {2025},
      note         = {This is an open access article under the CC BY license
                      (http://creativecommons.org/licenses/by/4.0/).},
      abstract     = {Radiation therapy can trigger activation of the cyclic
                      GMP-AMP synthase (cGAS)- Stimulator of interferon genes
                      (STING) axis via cytoplasmic dsDNA fragment induction. The
                      activation of cGAS-STING initiates innate immune signaling
                      mediated by interferon type I that can contribute to
                      eradicate the malignancy. The effect was shown to depend on
                      the fractionation scheme employed. We hypothesized that the
                      innate immune response can also depend on radiation quality
                      because densely ionizing radiation, such as carbon ions,
                      have different effects on DNA lesion quality.We exposed an
                      in vitro 4T1 breast cancer model to either photons or carbon
                      ions and measured the clonogenic survival of cells with the
                      colony-forming assay. The occurrence of cytosolic dsDNA
                      fragments was assessed via immunofluorescence, whereas the
                      expression and release of interferon-β by quantitative
                      reverse transcription polymerase chain reaction and
                      enzyme-linked immunosorbent assay. Bulk RNA sequencing was
                      used to investigate global radiation-induced changes in gene
                      expression.We show here that carbon ions induced a
                      significantly higher yield of cytosolic dsDNA fragments per
                      unit dose as compared to photons. The higher efficiency also
                      translated in expression and release of interferon-β by the
                      tumor cells. The rate of cytoplasmic dsDNA foci as well as
                      interferon-β release increased with doses up to 20 Gy and
                      no differences for a fractionation scheme (3 × 8 Gy) were
                      found as compared to the single high doses (20 or 24 Gy) of
                      photons.In conclusion, we found that the release of
                      interferon-β after radiation increases with the radiation
                      dose up to 20 Gy and that carbon ions have the potential to
                      elicit a strong innate immune signaling.},
      cin          = {BIO},
      ddc          = {610},
      cid          = {I:(DE-Ds200)BIO-20160831OR354},
      pnm          = {633 - Life Sciences – Building Blocks of Life: Structure
                      and Function (POF4-633) / FAIR Phase-0 - FAIR Phase-0
                      Research Program (GSI-FAIR-Phase-0) / SUC-GSI-Darmstadt -
                      Strategic university cooperation GSI-TU Darmstadt
                      (SUC-GSI-DA) / 50WB2014 - Molekulare Grundlagen der
                      Krebsentstehung durch kosmische Strahlung (BMWK-50WB2014) /
                      02NUK054A - Verbundprojekt VERCHROMT II: Erkennung,
                      Verarbeitung und biologische Konsequenzen von
                      Chromatinschäden nach Teilchenbestrahlung II, Teilprojekt A
                      (BMBF-02NUK054A) / BMBF-02NUK050A - Genetische Risiken und
                      entzündungshemmende Wirkung von dicht-ionisierender
                      alpha-Strahlung - Teilprojekt A (BMBF-02NUK050A)},
      pid          = {G:(DE-HGF)POF4-633 / G:(Ds200)GSI-FAIR-Phase-0 /
                      G:(DE-Ds200)SUC-GSI-DA / G:(DE-Ds200)BMWK-50WB2014 /
                      G:(DE-Ds200)BMBF-02NUK054A / G:(DE-Ds200)BMBF-02NUK050A},
      experiment   = {$EXP:(DE-Ds200)SBio_Jakob-20200803$ /
                      $EXP:(DE-Ds200)SBio_Fournier-20200803$},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {40486289},
      doi          = {10.1016/j.adro.2025.101783},
      url          = {https://repository.gsi.de/record/359584},
}