[68Ga]pentixafor for CXCR4 imaging in a PC-3 prostate cancer xenograft model – comparison with [18F]FDG PET/CT, MRI and ex vivo receptor expression
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Sarah M. Schwarzenböck1, Jan Stenzel2, Thomas Otto1, Heike V. Helldorff1, Carina Bergner1, Jens Kurth1, Stefan Polei2, Tobias Lindner2, Romina Rauer2, Alexander Hohn1, Oliver W. Hakenberg3, Hans J. Wester4, Brigitte Vollmar5 and Bernd J. Krause1
1Department of Nuclear Medicine, Rostock University Medical Centre, 18057 Rostock, Germany
2Core Facility Small Animal Imaging, Rostock University Medical Centre, 18057 Rostock, Germany
3Department of Urology, Rostock University Medical Centre, 18057 Rostock, Germany
4Institute for Radiopharmaceutical Chemistry, Technische Universität München, 85748 Garching, Germany
5Institute for Experimental Surgery, Rostock University Medical Centre, 18057 Rostock, Germany
Sarah M. Schwarzenböck, email: firstname.lastname@example.org
Keywords: prostate cancer; small animal PET/CT; [68Ga]Pentixafor; MRI; CXCR4
Received: March 10, 2017 Accepted: August 17, 2017 Published: September 16, 2017
Purpose: The aim was to characterize the properties of [68Ga]Pentixafor as tracer for prostate cancer imaging in a PC-3 prostate cancer xenograft mouse model and to investigate its correlation with [18F]FDG PET/CT, magnetic resonance imaging (MRI) and ex vivo analyses.
Methods: Static [68Ga]Pentixafor and [18F]FDG PET as well as morphological/ diffusion weighted MRI and 1H MR spectroscopy was performed. Imaging data were correlated with ex vivo biodistribution and CXCR4 expression in PC-3 tumors (immunohistochemistry (IHC), mRNA analysis). Flow cytometry was performed for evaluation of localization of CXCR4 receptors (in vitro PC-3 cell experiments).
Results: Tumor uptake of [68Ga]Pentixafor was significantly lower compared to [18F]FDG. Ex vivo CXCR4 mRNA expression of tumors was shown by PCR. Only faint tumor CXCR4 expression was shown by IHC (immuno reactive score of 3). Accordingly, flow cytometry of PC-3 cells revealed only a faint signal, cell membrane permeabilisation showed a slight signal increase. There was no significant correlation of [68Ga]Pentixafor tumor uptake and ex vivo receptor expression. Spectroscopy showed typical spectra of prostate cancer.
Conclusion: PC-3 tumor uptake of [68Ga]Pentixafor was existent but lower compared to [18F]FDG. No significant correlation of ex vivo tumor CXCR4 receptor expression and [68Ga]Pentixafor tumor uptake was shown. CXCR4 receptor expression on the surface of PC-3 cells was existent but rather low possibly explaining the limited [68Ga]Pentixafor tumor uptake; receptor localization in the interior of PC-3 cells is presumable as shown by cell membrane permeabilisation. Further studies are necessary to define the role of [68Ga]Pentixafor in prostate cancer imaging.
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