Auger electron-emitting EGFR-targeted and non-targeted [197Hg]Hg-gold nanoparticles for treatment of glioblastoma multiforme (GBM)

Abstract Background We describe here radiation nanomedicines for glioblastoma multiforme (GBM) composed of gold nanoparticles (AuNPs) that integrate the Auger electron-emitter, 197Hg. [197Hg]Hg-AuNPs were conjugated to anti-epidermal growth factor receptor (EGFR) panitumumab or were non-targeted. Ou...

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Main Authors: Madeline K. Brown, Zhongli Cai, Constantine J. Georgiou, Shaohuang Chen, Yumeela Ganga-Sah, Valery Radchenko, James T. Rutka, Raymond M. Reilly
Format: Article
Language:English
Published: SpringerOpen 2025-07-01
Series:EJNMMI Radiopharmacy and Chemistry
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Online Access:https://doi.org/10.1186/s41181-025-00367-2
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author Madeline K. Brown
Zhongli Cai
Constantine J. Georgiou
Shaohuang Chen
Yumeela Ganga-Sah
Valery Radchenko
James T. Rutka
Raymond M. Reilly
author_facet Madeline K. Brown
Zhongli Cai
Constantine J. Georgiou
Shaohuang Chen
Yumeela Ganga-Sah
Valery Radchenko
James T. Rutka
Raymond M. Reilly
author_sort Madeline K. Brown
collection DOAJ
description Abstract Background We describe here radiation nanomedicines for glioblastoma multiforme (GBM) composed of gold nanoparticles (AuNPs) that integrate the Auger electron-emitter, 197Hg. [197Hg]Hg-AuNPs were conjugated to anti-epidermal growth factor receptor (EGFR) panitumumab or were non-targeted. Our aim was to compare the cytotoxicity and DNA-damaging properties in vitro of panitumumab-[197Hg]Hg-AuNPs and non-targeted [197Hg]Hg-AuNPs on U251-Luc human GBM cells and estimate their cellular dosimetry. We further aimed to compare the biodistribution in vivo of panitumumab-[197Hg]Hg-AuNPs and [197Hg]Hg-AuNPs after convection-enhanced delivery (CED) in NRG mice with U251-Luc tumours in the brain and estimate the absorbed doses in the tumour and surrounding margins of healthy brain. Results [197Hg]Hg-AuNPs (26.8 ± 6.4 nm) were produced with a radiochemical yield of 98 ± 1% by incorporating 197Hg into the Turkevich synthesis method, forming a mercury-gold amalgam. Panitumumab-[197Hg]Hg-AuNPs exhibited high affinity (KD = 1.8 × 10–9 mol/L) binding to EGFR-positive U251-Luc cells. The binding of panitumumab-[197Hg]Hg-AuNPs to U251-Luc cells was 15-fold higher than [197Hg]Hg-AuNPs, and internalization and nuclear uptake were 12-fold and 18-fold greater, respectively. Panitumumab-[197Hg]Hg-AuNPs caused 84-fold more DNA double-strand breaks (DSBs) in U251-Luc cells than [197Hg]Hg-AuNPs. Panitumumab-[197Hg]Hg-AuNPs were ninefold more effective at reducing the clonogenic survival of U251-Luc cells than [197Hg]Hg-AuNPs. Panitumumab-[197Hg]Hg-AuNPs were twofold more cytotoxic than non-radioactive panitumumab-AuNPs (P = 0.04) and fivefold more cytotoxic than panitumumab (P = 0.01). The absorbed doses in the nucleus of U251-Luc cells treated in vitro with panitumumab-[197Hg]Hg-AuNPs or [197Hg]Hg-AuNPs were 8.8 ± 2.9 Gy and 0.6 ± 0.1 Gy, respectively. SPECT/CT imaging showed that panitumumab-[197Hg]Hg-AuNPs and [197Hg]Hg-AuNPs were strongly retained at the infusion site in the brain after CED up to 7 d in NRG mice with orthotopic U251-Luc tumours. Uptake of panitumumab-[197Hg]Hg-AuNPs in the tumour-bearing right hemisphere [484.5% injected dose/g (%ID/g)] was 172-fold and 579-fold greater than in the healthy left hemisphere and cerebellum, respectively. The uptake of [197Hg]Hg-AuNPs (423.9% ID/g) in the tumour-bearing right hemisphere was 85-fold and 64-fold higher than the left hemisphere and cerebellum, respectively. Most normal tissue uptake was < 1% ID/g, except for kidneys (9–20% ID/g), spleen (3.5–6.6% ID/g) and liver (0.6–3.3% ID/g). Dosimetry showed that 58% of the tumour received > 190 Gy for CED of 1.0 MBq of panitumumab-[197Hg]Hg-AuNPs vs. 0.6% of the tumour for non-targeted [197Hg]Hg-AuNPs, but both agents deposited > 50 Gy in 95% of the tumour. Doses decreased dramatically to 1.7 and 3.3 Gy at 1–3 mm from the tumour edge for panitumumab-[197Hg]Hg-AuNPs and [197Hg]Hg-AuNPs, respectively. Conclusion Radiation nanomedicines incorporating the AE-emitter, 197Hg administered by CED are a promising approach to treatment of GBM. Panitumumab-[197Hg]Hg-AuNPs are particularly attractive due to their EGFR-mediated binding, internalization and nuclear importation in GBM cells, which amplifies their in vitro cytotoxicity.
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spelling doaj-art-72c8e111adf84bf8a62b793a8611cb922025-08-20T03:46:12ZengSpringerOpenEJNMMI Radiopharmacy and Chemistry2365-421X2025-07-0110112010.1186/s41181-025-00367-2Auger electron-emitting EGFR-targeted and non-targeted [197Hg]Hg-gold nanoparticles for treatment of glioblastoma multiforme (GBM)Madeline K. Brown0Zhongli Cai1Constantine J. Georgiou2Shaohuang Chen3Yumeela Ganga-Sah4Valery Radchenko5James T. Rutka6Raymond M. Reilly7Department of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, University of TorontoDepartment of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, University of TorontoDepartment of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, University of TorontoLife Sciences Division, TRIUMFLife Sciences Division, TRIUMFLife Sciences Division, TRIUMFDivision of Neurosurgery, The Hospital for Sick ChildrenDepartment of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, University of TorontoAbstract Background We describe here radiation nanomedicines for glioblastoma multiforme (GBM) composed of gold nanoparticles (AuNPs) that integrate the Auger electron-emitter, 197Hg. [197Hg]Hg-AuNPs were conjugated to anti-epidermal growth factor receptor (EGFR) panitumumab or were non-targeted. Our aim was to compare the cytotoxicity and DNA-damaging properties in vitro of panitumumab-[197Hg]Hg-AuNPs and non-targeted [197Hg]Hg-AuNPs on U251-Luc human GBM cells and estimate their cellular dosimetry. We further aimed to compare the biodistribution in vivo of panitumumab-[197Hg]Hg-AuNPs and [197Hg]Hg-AuNPs after convection-enhanced delivery (CED) in NRG mice with U251-Luc tumours in the brain and estimate the absorbed doses in the tumour and surrounding margins of healthy brain. Results [197Hg]Hg-AuNPs (26.8 ± 6.4 nm) were produced with a radiochemical yield of 98 ± 1% by incorporating 197Hg into the Turkevich synthesis method, forming a mercury-gold amalgam. Panitumumab-[197Hg]Hg-AuNPs exhibited high affinity (KD = 1.8 × 10–9 mol/L) binding to EGFR-positive U251-Luc cells. The binding of panitumumab-[197Hg]Hg-AuNPs to U251-Luc cells was 15-fold higher than [197Hg]Hg-AuNPs, and internalization and nuclear uptake were 12-fold and 18-fold greater, respectively. Panitumumab-[197Hg]Hg-AuNPs caused 84-fold more DNA double-strand breaks (DSBs) in U251-Luc cells than [197Hg]Hg-AuNPs. Panitumumab-[197Hg]Hg-AuNPs were ninefold more effective at reducing the clonogenic survival of U251-Luc cells than [197Hg]Hg-AuNPs. Panitumumab-[197Hg]Hg-AuNPs were twofold more cytotoxic than non-radioactive panitumumab-AuNPs (P = 0.04) and fivefold more cytotoxic than panitumumab (P = 0.01). The absorbed doses in the nucleus of U251-Luc cells treated in vitro with panitumumab-[197Hg]Hg-AuNPs or [197Hg]Hg-AuNPs were 8.8 ± 2.9 Gy and 0.6 ± 0.1 Gy, respectively. SPECT/CT imaging showed that panitumumab-[197Hg]Hg-AuNPs and [197Hg]Hg-AuNPs were strongly retained at the infusion site in the brain after CED up to 7 d in NRG mice with orthotopic U251-Luc tumours. Uptake of panitumumab-[197Hg]Hg-AuNPs in the tumour-bearing right hemisphere [484.5% injected dose/g (%ID/g)] was 172-fold and 579-fold greater than in the healthy left hemisphere and cerebellum, respectively. The uptake of [197Hg]Hg-AuNPs (423.9% ID/g) in the tumour-bearing right hemisphere was 85-fold and 64-fold higher than the left hemisphere and cerebellum, respectively. Most normal tissue uptake was < 1% ID/g, except for kidneys (9–20% ID/g), spleen (3.5–6.6% ID/g) and liver (0.6–3.3% ID/g). Dosimetry showed that 58% of the tumour received > 190 Gy for CED of 1.0 MBq of panitumumab-[197Hg]Hg-AuNPs vs. 0.6% of the tumour for non-targeted [197Hg]Hg-AuNPs, but both agents deposited > 50 Gy in 95% of the tumour. Doses decreased dramatically to 1.7 and 3.3 Gy at 1–3 mm from the tumour edge for panitumumab-[197Hg]Hg-AuNPs and [197Hg]Hg-AuNPs, respectively. Conclusion Radiation nanomedicines incorporating the AE-emitter, 197Hg administered by CED are a promising approach to treatment of GBM. Panitumumab-[197Hg]Hg-AuNPs are particularly attractive due to their EGFR-mediated binding, internalization and nuclear importation in GBM cells, which amplifies their in vitro cytotoxicity.https://doi.org/10.1186/s41181-025-00367-2Glioblastoma multiforme (GBM)Gold nanoparticles197HgAuger electronsPanitumumabEpidermal growth factor receptors (EGFR)
spellingShingle Madeline K. Brown
Zhongli Cai
Constantine J. Georgiou
Shaohuang Chen
Yumeela Ganga-Sah
Valery Radchenko
James T. Rutka
Raymond M. Reilly
Auger electron-emitting EGFR-targeted and non-targeted [197Hg]Hg-gold nanoparticles for treatment of glioblastoma multiforme (GBM)
EJNMMI Radiopharmacy and Chemistry
Glioblastoma multiforme (GBM)
Gold nanoparticles
197Hg
Auger electrons
Panitumumab
Epidermal growth factor receptors (EGFR)
title Auger electron-emitting EGFR-targeted and non-targeted [197Hg]Hg-gold nanoparticles for treatment of glioblastoma multiforme (GBM)
title_full Auger electron-emitting EGFR-targeted and non-targeted [197Hg]Hg-gold nanoparticles for treatment of glioblastoma multiforme (GBM)
title_fullStr Auger electron-emitting EGFR-targeted and non-targeted [197Hg]Hg-gold nanoparticles for treatment of glioblastoma multiforme (GBM)
title_full_unstemmed Auger electron-emitting EGFR-targeted and non-targeted [197Hg]Hg-gold nanoparticles for treatment of glioblastoma multiforme (GBM)
title_short Auger electron-emitting EGFR-targeted and non-targeted [197Hg]Hg-gold nanoparticles for treatment of glioblastoma multiforme (GBM)
title_sort auger electron emitting egfr targeted and non targeted 197hg hg gold nanoparticles for treatment of glioblastoma multiforme gbm
topic Glioblastoma multiforme (GBM)
Gold nanoparticles
197Hg
Auger electrons
Panitumumab
Epidermal growth factor receptors (EGFR)
url https://doi.org/10.1186/s41181-025-00367-2
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