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Radiation Protection Dosimetry Advance Access originally published online on February 6, 2007
Radiation Protection Dosimetry 2006 122(1-4):521-527; doi:10.1093/rpd/ncl448
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

INVITED PAPER

Challenges and progress in predicting biological responses to incorporated radioactivity

R. W. Howell1,*, P. V. S. V. Neti1, M. Pinto1, B. I. Gerashchenko1, V. R. Narra2 and E. I. Azzam1

1 Department of Radiology, UMDNJ–New Jersey Medical School, Newark, NJ 07103, USA
2 Department of Radiation Oncology, The Cancer Institute of New Jersey, UMDNJ–Robert Wood Johnson Medical School, New Brunswick, NJ 08854, USA

*Corresponding author: rhowell{at}umdnj.edu


  Abstract

Prediction of risks and therapeutic outcome in nuclear medicine largely rely on calculation of the absorbed dose. Absorbed dose specification is complex due to the wide variety of radiations emitted, non-uniform activity distribution, biokinetics, etc. Conventional organ absorbed dose estimates assumed that radioactivity is distributed uniformly throughout the organ. However, there have been dramatic improvements in dosimetry models that reflect the substructure of organs as well as tissue elements within them. These models rely on improved nuclear medicine imaging capabilities that facilitate determination of activity within voxels that represent tissue elements of ~0.2–1 cm3. However, even these improved approaches assume that all cells within the tissue element receive the same dose. The tissue element may be comprised of a variety of cells having different radiosensitivities and different incorporated radioactivity. Furthermore, the extent to which non-uniform distributions of radioactivity within a small tissue element impact the absorbed dose distribution is strongly dependent on the number, type, and energy of the radiations emitted by the radionuclide. It is also necessary to know whether the dose to a given cell arises from radioactive decays within itself (self-dose) or decays in surrounding cells (cross-dose). Cellular response to self-dose can be considerably different than its response to cross-dose from the same radiopharmaceutical. Bystander effects can also play a role in the response. Evidence shows that even under conditions of ‘uniform’ distribution of radioactivity, a combination of organ dosimetry, voxel dosimetry and dosimetry at the cellular and multicellular levels can be required to predict response.


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