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Limitations of dynamic contrast‐enhanced MRI in monitoring radiation‐induced changes in the fraction of radiobiologically hypoxic cells in human melanoma xenografts
Author(s) -
Benjaminsen Ilana C.,
Melås Elin A.,
Mathiesen Berit S.,
Rofstad Einar K.
Publication year - 2008
Publication title -
journal of magnetic resonance imaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.563
H-Index - 160
eISSN - 1522-2586
pISSN - 1053-1807
DOI - 10.1002/jmri.21602
Subject(s) - nuclear medicine , magnetic resonance imaging , radiation therapy , melanoma , medicine , irradiation , perfusion , pathology , chemistry , cancer research , radiology , physics , nuclear physics
Purpose To investigate the potential of gadopentetate dimeglumine (Gd‐DTPA)‐based dynamic contrast‐enhanced magnetic resonance imaging (DCE‐MRI) in detecting radiation‐induced changes in the fraction of radiobiologically hypoxic cells in A‐07 human melanoma xenografts. Materials and Methods A‐07 tumors were randomly assigned to an unirradiated control group or a group given a single radiation dose of 20 Gy. DCE‐MRI and measurement of fraction of hypoxic cells were performed immediately before and 24 h after the radiation exposure. Tumor images of E · F ( E is the initial extraction fraction of Gd‐DTPA and F is blood perfusion) and λ (λ is proportional to extracellular volume fraction) were produced by subjecting DCE‐MRI series to Kety analysis. Fraction of hypoxic cells was measured by using a radiobiological assay based on the paired survival curve method. Results Fraction of radiobiologically hypoxic cells was higher in irradiated tumors (26.2 ± 5.8%) than in unirradiated tumors (7.5 ± 2.7%) by a factor of 3.5 ± 1.5 ( P = 0.0093), whereas only minor radiation‐induced changes in E · F and λ could be detected. Conclusion DCE‐MRI does not seem to offer insight into the changes in fraction of radiobiologically hypoxic cells occurring in A‐07 tumors within 24 h after irradiation with 20 Gy. J. Magn. Reson. Imaging 2008;28:1209–1218. © 2008 Wiley‐Liss, Inc.