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@ARTICLE{Swartz:284783,
      author       = {H. M. Swartz and P. Vaupel$^*$ and A. B. Flood},
      title        = {{A} {C}ritical {A}nalysis of {P}ossible {M}echanisms for
                      the {O}xygen {E}ffect in {R}adiation {T}herapy with
                      {FLASH}.},
      journal      = {Advances in experimental medicine and biology},
      volume       = {1438},
      issn         = {0065-2598},
      address      = {[Heidelberg]},
      publisher    = {Springer},
      reportid     = {DKFZ-2023-02094},
      isbn         = {978-3-031-42002-3 (print)},
      pages        = {127-133},
      year         = {2023},
      abstract     = {The aim of this review is to stimulate readers to undertake
                      appropriate investigations of the mechanism for a possible
                      oxygen effect in FLASH. FLASH is a method of delivery of
                      radiation that empirically, in animal models, appears to
                      decrease the impact of radiation on normal tissues while
                      retaining full effect on tumors. This has the potential for
                      achieving a significantly increased effectiveness of
                      radiation therapy. The mechanism is not known but,
                      especially in view of the prominent role that oxygen has in
                      the effects of radiation, investigations of mechanisms of
                      FLASH have often focused on impacts of FLASH on oxygen
                      levels. We and others have previously shown that simple
                      differential depletion of oxygen directly changing the
                      response to radiation is not a likely mechanism. In this
                      review we consider how time-varying changes in oxygen levels
                      could account for the FLASH effect by changing
                      oxygen-dependent signaling in cells. While the methods of
                      delivering FLASH are still evolving, current approaches for
                      FLASH can differ from conventional irradiation in several
                      ways that can impact the pattern of oxygen consumption: the
                      rate of delivery of the radiation (40 Gy/s vs. 0.1 Gy/s),
                      the time over which each fraction is delivered (e.g., <0.5
                      s. vs. 300 s), the delivery in pulses, the number of
                      fractions, the size of the fractions, and the total duration
                      of treatment. Taking these differences into account and
                      recognizing that cell signaling is an intrinsic component of
                      the need for cells to maintain steady-state conditions and,
                      therefore, is activated by small changes in the environment,
                      we delineate the potential time dependent changes in oxygen
                      consumption and overview the cell signaling pathways whose
                      differential activation by FLASH could account for the
                      observed biological effects of FLASH. We speculate that the
                      most likely pathways are those involved in repair of damaged
                      DNA.},
      keywords     = {Cancer (Other) / DNA damage repair (Other) / FLASH (Other)
                      / Radiation therapy (Other)},
      cin          = {FR01},
      ddc          = {570},
      cid          = {I:(DE-He78)FR01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)3 / PUB:(DE-HGF)16},
      pubmed       = {pmid:37845451},
      doi          = {DOI:10.1007/978-3-031-42003-0_21},
      url          = {https://inrepo02.dkfz.de/record/284783},
}