3051 Background: This study assesses early vascular effects of SU in RCC pts with DCE-MRI and DWI at 3T. Methods: In 8 pts with abdominal RCC lesions, we performed 3T DCE-MRI and DWI at baseline, on d3 and d10 after start of SU. For DWI we used three gradient factors (b50-300-600 s/mm2). Apparent diffusion coefficient (ADC) maps were calculated for tumor and healthy liver tissue. DCE-MRI was performed after an iv bolus of Gadolinium (Gd)-DTPA using fast T1 measurements for 5 min. Mean kep and Ktrans were calculated and histogram analysis was performed. Tumor perfusion was measured after a second bolus of Gd-DTPA by dynamic T2* weighted measurements during 90 sec. VEGF plasma levels were measured on d0, d3 and d10. Results: In 8 RCC pts, SU did not result in significant changes in mean kep (s-1) and Ktrans (s-1) values in tumors or healthy liver tissue on d3 and d10. However, in 6 pts, the differences in mean kep values in tumors at d10 exceeded the repeatability coefficient. No significant kep and Ktrans histogram shift in tumor or healthy liver ROIs was observed. Two pts showed an increase in tumor mean kep values, one with objective progressive disease. All other pts had stable disease after 2 cycles of SU. In 2 pts a remarkable increase in kep values was observed in healthy liver tissue while in tumors their kep values decreased. Interestingly, ADC (x10-6 s/mm2) increased from baseline (mean 1174, range 868-1373) to d3 (mean 1315, range 1008-2097, p=0.036) and decreased to d10 (mean 1154, range 824-2005, p=0.029). D0 and d10 ADC values did not differ (p >0.1). This indicates enhanced Brownian movements of water molecules, possibly due to development of edema en necrosis which recovers at d10 due to loss of edema or organization of necrosis. VEGF plasma levels increased from baseline to day 10 (mean 0.55 ng/ml to 1.24 ng/ml, p=0.062). Conclusions: This is the first report of DWI at 3T in SU-treated RCC pts. SU significantly increased ADC at d3, with recurrence to baseline values at d10, possibly due to the development of edema and necrosis. DWI may serve as a potential biomarker for the effect of angiogenesis inhibitors. No significant financial relationships to disclose.
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