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Diffusion-weighted MR Imaging in Monitoring the Effect of a Vascular Targeting Agent on Rhabdomyosarcoma in Rats¹

¹ From the Departments of Radiology (H.C.T., F.D.K., F.C., Y.N., H.B., G.M., R.H.), Experimental Radiobiology/Laboratory of Experimental Oncology (W.L.), and Pathology (E.K.V.), University Hospitals Leuven, Herestraat 49, B-3000 Leuven, Belgium; and Department of Radiology, Zhong Da Hospital, Southeast University, Nanjing, China (F.C.). Received October 24, 2003; revision requested January 13, 2004; final revision received May 19; accepted June 17. H.C.T. supported by a grant from the Bernese Cancer League and by the Kurt and Senta Hermann Foundation. Address correspondence to Y.N. (e-mail: yicheng.ni@med.kuleuven.ac.be).

PURPOSE: To evaluate diffusion-weighted magnetic resonance (MR) imaging for monitoring tumor response in rats after administration of combretastatin A4 phosphate.

MATERIALS AND METHODS: Study protocol was approved by local ethical committee for animal care and use. Rhabdomyosarcomas implanted subcutaneously in both flanks of 17 rats were evaluated with 1.5-T MR unit by using four-channel wrist coil. Transverse T2-weighted fast spin-echo sequences, T1-weighted spin-echo sequences before and after gadodiamide administration, and transverse echo-planar diffusion-weighted MR examinations were performed before, 1 and 6 hours, and 2 and 9 days after intraperitoneal injection of vascular targeting agent (combretastatin A4 phosphate, 25 mg/kg). Apparent diffusion coefficient (ADC) was automatically calculated from diffusion-weighted MR imaging findings. These findings were compared with histopathologic results at each time point. For statistical analysis, paired Student t tests with Bonferroni correction for multiple testing were used.

RESULTS: T1-weighted images before combretastatin administration showed enhancement of solid tumor tissue but not of central necrosis. At 1 and 6 hours after combretastatin injection, enhancement of solid tissue disappeared almost completely, with exception of small peripheral rim. At 2 and 9 days after combretastatin injection, enhancement progressively reappeared in tumor periphery. ADC, however, showed decrease early after combretastatin injection ([1.26 ± 0.16]x 10^–3 mm²/sec before, [1.18 ± 0.17]x 10^–3 mm²/sec 1 hour after [P = .0005] and [1.08 ± 0.14]x 10^–3 mm²/sec 6 hours after [P = .0007] combretastatin A4 phosphate injection), histologically corresponding to vessel congestion and vascular shutdown in periphery but no necrosis. An increase of ADC ([1.79 ± 0.13]x 10^–3 mm²/sec) (P < .0001) 2 days after combretastatin A4 phosphate injection was paralleled by progressive histologic necrosis. A significant (P < .0001) decrease in ADC 9 days after treatment ([1.41 ± 0.15]x 10^–3 mm²/sec) corresponded to tumor regrowth.

CONCLUSION: In addition to basic relaxation-weighted MR imaging and postgadolinium T1-weighted MR imaging to enable prompt detection of vascular shutdown, diffusion-weighted MR imaging was used to discriminate between nonperfused but viable and necrotic tumor tissues for early monitoring of therapeutic effects of vascular targeting agent.

© RSNA, 2005

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