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• W4387568314 abstract "Glypican-1 (GPC1) is overexpressed in several solid cancers and is associated with tumor progression, whereas its expression is low in normal tissues. This study aimed to evaluate the potential of an anti-GPC1 monoclonal antibody (GPC1 mAb) labeled with ⁸⁹Zr or ²¹¹At as a theranostic target in pancreatic ductal adenocarcinoma. <b>Methods:</b> GPC1 mAb clone 01a033 was labeled with ⁸⁹Zr or ²¹¹At with a deferoxamine or decaborane linker, respectively. The internalization ability of GPC1 mAb was evaluated by fluorescence conjugation using a confocal microscope. PANC-1 xenograft mice (<i>n</i> = 6) were intravenously administered [⁸⁹Zr]GPC1 mAb (0.91 ± 0.10 MBq), and PET/CT scanning was performed for 7 d. Uptake specificity was confirmed through a comparative study using GPC1-positive (BxPC-3) and GPC1-negative (BxPC-3 GPC1-knockout) xenografts (each <i>n</i> = 3) and a blocking study. DNA double-strand breaks were evaluated using the γH2AX antibody. The antitumor effect was evaluated by administering [²¹¹At]GPC1 mAb (∼100 kBq) to PANC-1 xenograft mice (<i>n</i> = 10). <b>Results:</b> GPC1 mAb clone 01a033 showed increased internalization ratios over time. One day after administration, a high accumulation of [⁸⁹Zr]GPC1 mAb was observed in the PANC-1 xenograft (SUV_max, 3.85 ± 0.10), which gradually decreased until day 7 (SUV_max, 2.16 ± 0.30). The uptake in the BxPC-3 xenograft was significantly higher than in the BxPC-3 GPC1-knockout xenograft (SUV_max, 4.66 ± 0.40 and 2.36 ± 0.36, respectively; <i>P</i> = 0.05). The uptake was significantly inhibited in the blocking group compared with the nonblocking group (percentage injected dose per gram, 7.3 ± 1.3 and 12.4 ± 3.0, respectively; <i>P</i> = 0.05). DNA double-strand breaks were observed by adding 150 kBq of [²¹¹At]GPC1 and were significantly suppressed by the internalization inhibitor (dynasore), suggesting a substantial contribution of the internalization ability to the antitumor effect. Tumor growth suppression was observed in PANC-1 mice after the administration of [²¹¹At]GPC1 mAb. Internalization inhibitors (prochlorperazine) significantly inhibited the therapeutic effect of [²¹¹At]GPC1 mAb, suggesting an essential role in targeted α-therapy. <b>Conclusion:</b> [⁸⁹Zr]GPC1 mAb PET showed high tumoral uptake in the early phase after administration, and targeted α-therapy using [²¹¹At]GPC1 mAb showed tumor growth suppression. GPC1 is a promising target for future applications for the precise diagnosis of pancreatic ductal adenocarcinoma and GPC1-targeted theranostics." @default.
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• W4387568314 date "2023-10-12" @default.
• W4387568314 modified "2023-10-17" @default.
• W4387568314 title "Immuno-PET and Targeted α-Therapy Using Anti–Glypican-1 Antibody Labeled with⁸⁹Zr or²¹¹At: A Theranostic Approach for Pancreatic Ductal Adenocarcinoma" @default.
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• W4387568314 doi "https://doi.org/10.2967/jnumed.123.266313" @default.
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