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@ARTICLE{Storey:186670,
      author       = {C. M. Storey and M. Altai and M. Bicak and D. R. Veach and
                      K. Lueckerath$^*$ and G. Adrian and M. R. McDevitt and T.
                      Kalidindi and J. E. Park and K. Herrmann$^*$ and D. Abou and
                      W. Zedan and N. Peekhaus and R. J. Klein and R. Damoiseaux
                      and S. M. Larson and H. Lilja and D. Thorek and D. Ulmert},
      title        = {{Q}uantitative {I}n {V}ivo {I}maging of the {A}ndrogen
                      {R}eceptor {A}xis {R}eveals {D}egree of {P}rostate {C}ancer
                      {R}adiotherapy {R}esponse.},
      journal      = {Molecular cancer research},
      volume       = {21},
      number       = {4},
      issn         = {1541-7786},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2023-00039},
      pages        = {307-315},
      year         = {2023},
      note         = {2023 Apr 1;21(4):307-315},
      abstract     = {Non-invasive biomarkers for androgen receptor (AR) pathway
                      activation are urgently needed to better monitor patient
                      response to prostate cancer (PCa) therapies. AR is a
                      critical driver and mediator of resistance of PCa but
                      currently available non-invasive PCa biomarkers to monitor
                      AR activity are discordant with downstream AR pathway
                      activity. External beam radiotherapy (EBRT) remains a common
                      treatment for all stages of PCa, and DNA damage induced by
                      EBRT upregulates AR pathway activity to promote therapeutic
                      resistance. [89Zr]11B6-PET is a novel modality targeting
                      prostate-specific protein human kallikrein 2 (hK2), which is
                      a surrogate biomarker for AR activity. Here, we studied if
                      $[\&sup89;Zr]11B6-PET$ can accurately assess EBRT-induced AR
                      activity. Genetic and human PCa mouse models received EBRT
                      (2-50 Gy) and treatment response was monitored by
                      [89Zr]11B6-PET/CT. Radiotracer uptake and expression of AR
                      and AR target genes was quantified in resected tissue. EBRT
                      increased AR pathway activity and $[\&sup89;Zr]11B6$ uptake
                      in LNCaP-AR and 22RV1 tumors. EBRT increased
                      prostate-specific $[\&sup89;Zr]11B6$ uptake in PCa-bearing
                      mice (Hi-Myc x $Pb_KLK2)$ with no significant changes in
                      uptake in healthy $(Pb_KLK2)$ mice, and this correlated with
                      hK2 protein levels. Implications: hK2 expression in PCa
                      tissue is a proxy of EBRT-induced AR activity that can
                      non-invasively be detected using $[\&sup89;Zr]11B6-PET;$
                      further clinical evaluation of hK2-PET for monitoring
                      response and development of resistance to EBRT in real time
                      is warranted.},
      cin          = {ED01},
      ddc          = {610},
      cid          = {I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36608299},
      doi          = {10.1158/1541-7786.MCR-22-0736},
      url          = {https://inrepo02.dkfz.de/record/186670},
}