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@ARTICLE{Bonekamp:119319,
      author       = {D. Bonekamp$^*$ and K. Mouridsen and A. Radbruch$^*$ and F.
                      T. Kurz$^*$ and O. Eidel and A. Wick and H.-P. Schlemmer$^*$
                      and W. Wick$^*$ and M. Bendszus and L. Østergaard and P.
                      Kickingereder$^*$},
      title        = {{A}ssessment of tumor oxygenation and its impact on
                      treatment response in bevacizumab-treated recurrent
                      glioblastoma.},
      journal      = {Journal of cerebral blood flow $\&$ metabolism},
      volume       = {37},
      number       = {2},
      issn         = {1559-7016},
      address      = {Thousands Oaks, Calilf.},
      publisher    = {Sage},
      reportid     = {DKFZ-2017-00074},
      pages        = {485 - 494},
      year         = {2017},
      abstract     = {Antiantiogenic therapy with bevacizumab in recurrent
                      glioblastoma is currently understood to both reduce
                      microvascular density and to prune abnormal tumor
                      microvessels. Microvascular pruning and the resulting
                      vascular normalization are hypothesized to reduce tumor
                      hypoxia and increase supply of systemic therapy to the
                      tumor; however, the underlying pathophysiological changes
                      and their timing after treatment initiation remain
                      controversial. Here, we use a novel dynamic susceptibility
                      contrast MRI-based method, which allows simultaneous
                      assessment of tumor net oxygenation changes reflected by the
                      tumor metabolic rate of oxygen and vascular normalization
                      represented by the capillary transit time heterogeneity. We
                      find that capillary transit time heterogeneity, and hence
                      the oxygen extraction fraction combine with the tumoral
                      blood flow (cerebral blood flow) in such a way that the
                      overall tumor oxygenation appears to be worsened despite
                      vascular normalization. Accordingly, hazards for both
                      progression and death are found elevated in patients with a
                      greater reduction of tumor metabolic rate of oxygen in
                      response to bevacizumab and patients with higher
                      intratumoral tumor metabolic rate of oxygen at baseline.
                      This implies that tumors with a higher degree of
                      angiogenesis prior to bevacizumab-treatment retain a higher
                      level of angiogenesis during therapy despite a greater
                      antiangiogenic effect of bevacizumab, hinting at evasive
                      mechanisms limiting bevacizumab efficacy in that a reversal
                      of their biological behavior and relative prognosis does not
                      occur.},
      cin          = {E010 / G370 / E012},
      ddc          = {610},
      cid          = {I:(DE-He78)E010-20160331 / I:(DE-He78)G370-20160331 /
                      I:(DE-He78)E012-20160331},
      pnm          = {315 - Imaging and radiooncology (POF3-315)},
      pid          = {G:(DE-HGF)POF3-315},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26861817},
      doi          = {10.1177/0271678X16630322},
      url          = {https://inrepo02.dkfz.de/record/119319},
}