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@ARTICLE{Saager:157104,
      author       = {M. Saager$^*$ and E. W. Hahn and P. Peschke$^*$ and S.
                      Brons and P. E. Huber$^*$ and J. Debus$^*$ and C.
                      Karger$^*$},
      title        = {{R}amipril reduces incidence and prolongates latency time
                      of radiation-induced rat myelopathy after photon and carbon
                      ion irradiation.},
      journal      = {Journal of radiation research},
      volume       = {61},
      number       = {5},
      issn         = {1349-9157},
      address      = {[Oxford]},
      publisher    = {Oxford University Press},
      reportid     = {DKFZ-2020-01395},
      pages        = {791-798},
      year         = {2020},
      note         = {2020 Sep 8;61(5):791-798#EA:E040#LA:E040#},
      abstract     = {To test the hypothesis that the use of an
                      angiotensin-converting enzyme inhibitor (ACEi) during
                      radiotherapy may be ameliorative for treatment-related
                      normal tissue damage, a pilot study was conducted with the
                      clinically approved (ACE) inhibitor ramipril on the outcome
                      of radiation-induced myelopathy in the rat cervical spinal
                      cord model. Female Sprague Dawley rats were irradiated with
                      single doses of either carbon ions (LET 45 keV/μm) at the
                      center of a 6 cm spread-out Bragg peak (SOBP) or 6 MeV
                      photons. The rats were randomly distributed into 4
                      experimental arms: (i) photons; (ii) photons + ramipril;
                      (iii) carbon ions and (iv) carbon ions + ramipril. Ramipril
                      administration (2 mg/kg/day) started directly after
                      irradiation and was maintained during the entire follow-up.
                      Complete dose-response curves were generated for the
                      biological endpoint radiation-induced myelopathy (paresis
                      grade II) within an observation time of 300 days.
                      Administration of ramipril reduced the rate of paralysis at
                      high dose levels for photons and for the first time a
                      similar finding for high-LET particles was demonstrated,
                      which indicates that the effect of ramipril is independent
                      from radiation quality. The reduced rate of myelopathy is
                      accompanied by a general prolongation of latency time for
                      photons and for carbon ions. Although the already clinical
                      approved drug ramipril can be considered as a mitigator of
                      radiation-induced normal tissue toxicity in the central
                      nervous system, further examinations of the underlying
                      pathological mechanisms leading to radiation-induced
                      myelopathy are necessary to increase and sustain its
                      mitigative effectiveness.},
      cin          = {E040 / E050 / E055},
      ddc          = {610},
      cid          = {I:(DE-He78)E040-20160331 / I:(DE-He78)E050-20160331 /
                      I:(DE-He78)E055-20160331},
      pnm          = {315 - Imaging and radiooncology (POF3-315)},
      pid          = {G:(DE-HGF)POF3-315},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32657322},
      doi          = {10.1093/jrr/rraa042},
      url          = {https://inrepo02.dkfz.de/record/157104},
}