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@ARTICLE{Bakos:310089,
      author       = {G. Bakos$^*$ and U. Bauder-Wüst$^*$ and J. Landry and M.
                      Roscher$^*$ and B. Ramasz and F. Bruchertseifer and A.
                      Morgenstern and C. Kratochwil and V. Beneš and M.
                      Benesova-Schäfer$^*$},
      title        = {{E}p{CAM}-{PSMA}: {P}otential predictors of treatment
                      outcomes for {PSMA}-targeted alpha therapies in metastatic
                      castration-resistant prostate cancer.},
      journal      = {Molecular therapy. Oncology.},
      volume       = {34},
      number       = {1},
      address      = {[New York]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2026-00433},
      pages        = {201143},
      year         = {2026},
      note         = {Molecular Therapy. Oncology. = 2950-3299 /
                      #EA:E270#LA:E270#},
      abstract     = {Targeted radionuclide therapy and targeted alpha therapy
                      directed at prostate-specific membrane antigen (PSMA)
                      represent emerging treatment modalities for metastatic
                      castration-resistant prostate cancer (mCRPC). However,
                      therapeutic resistance remains a significant barrier to
                      their clinical success. We discovered that dynamic changes
                      in cell surface levels of epithelial cell adhesion molecule
                      (EpCAM) and PSMA can serve as predictive biomarkers in
                      late-stage mCRPC patients treated with the
                      beta-minus-particle-emitting [177Lu]Lu-PSMA-617, in
                      combination with the alpha-particle-emitting
                      [225Ac]Ac-PSMA-617, and we further explored the underlying
                      molecular mechanisms. Using flow cytometry to profile EpCAM
                      and PSMA on circulating tumor cells (CTCs), we observed that
                      Nonresponders displayed significantly higher EpCAM and lower
                      PSMA levels than Responders, both at baseline and after the
                      first treatment cycle. Over subsequent cycles, both markers
                      declined in Nonresponders, whereas Responder CTCs maintained
                      EpCAM expression but progressively lost PSMA. Transcriptome
                      analysis identified upregulation of hub genes involved in
                      the regulation of key pathways such as enhanced DNA-damage
                      repair, anti-apoptotic activity, increased tumor cell
                      growth, and altered surface marker trafficking and
                      recycling, potentially driving EpCAM-PSMA dynamics and
                      contributing to therapy resistance. Ultimately, integrating
                      surface-marker-driven treatment response predictions with
                      novel treatment strategies may help to overcome treatment
                      resistance in mCRPC.},
      keywords     = {CTCs (Other) / EpCAM (Other) / PSMA (Other) / TαT (Other)
                      / circulating tumor cells (Other) / epithelial cell adhesion
                      molecule (Other) / gene expression analysis (Other) / liquid
                      biopsy (Other) / mCRPC (Other) / metastatic
                      castration-resistant prostate cancer (Other) /
                      prostate-specific membrane antigen (Other) / surface marker
                      dynamics (Other) / targeted alpha therapy (Other) /
                      treatment resistance (Other) / treatment response prediction
                      (Other)},
      cin          = {E270 / W630},
      cid          = {I:(DE-He78)E270-20160331 / I:(DE-He78)W630-20160331},
      pnm          = {315 - Bildgebung und Radioonkologie (POF4-315)},
      pid          = {G:(DE-HGF)POF4-315},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41732759},
      pmc          = {pmc:PMC12925578},
      doi          = {10.1016/j.omton.2026.201143},
      url          = {https://inrepo02.dkfz.de/record/310089},
}