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Radiation-Induced Biologic Bystander Effect Elicited In Vitro by Targeted Radiopharmaceuticals Labeled with {alpha}-, ß-, and Auger Electron–Emitting Radionuclides

Marie Boyd1, Susan C. Ross1, Jennifer Dorrens1,2, Natasha E. Fullerton1, Ker Wei Tan3, Michael R. Zalutsky2 and Robert J. Mairs1,4

1 Targeted Therapy Group, Division of Cancer Science and Molecular Pathology, Glasgow University, Cancer Research United Kingdom Beatson Laboratories, Glasgow, United Kingdom; 2 Department of Radiology, Duke University Medical Center, Durham, North Carolina; 3 Glasgow University School for Cancer Studies, Cancer Research United Kingdom Beatson Laboratories, Glasgow, United Kingdom; and 4 Department of Child Health, Yorkhill Hospital, Glasgow, United Kingdom


Figure 1
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  		FIGURE 1.  131I-MIBG uptake by UVW cells and EJ138 cells, untransfected and transfected with the NAT gene. Uptake evaluation was performed after administration of 7 kBq 131I-MIBG in the presence or absence of 1.5 mmol/L DMI, a specific inhibitor of NAT-mediated uptake. Data are mean ± SD of 3 experiments performed in triplicate.

 

Figure 2
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  		FIGURE 2.  Uptake of 131I-MIBG over a range of activity concentrations by UVW cells and EJ138 cells transfected with NAT gene. Data are mean ± SD of 3 experiments performed in triplicate.

 

Figure 3
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  		FIGURE 3.  Survival of UVW/NAT cells (A) and EJ138/NAT cells (B) after treatment with {gamma}-radiation or medium from irradiated cells. Data are mean ± SD of 6 experiments performed in triplicate.

 

Figure 4
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  		FIGURE 4.  Survival of UVW/NAT cells (A) and EJ138/NAT cells (B) after treatment with 131I-MIBG or medium from 131I-MIBG-treated cells. Data are mean ± SD of 6 experiments performed in triplicate.

 

Figure 5
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  		FIGURE 5.  Survival of UVW/NAT cells (A and B) and EJ138/NAT cells (C and D) after treatment with 123I-MIBG and 211At-MABG, respectively, or medium from radiopharmaceutical-treated cells. Data are mean ± SD of 6 experiments performed in triplicate.

 




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