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1-¹¹C-Acetate Kinetics of Prostate Cancer

¹ Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, California; ² Radiology, School of Medicine, University of California, San Diego, California; and ³ Nuclear Medicine, Katholieke Universiteit, Leuven, Belgium

Correspondence: For correspondence or reprints contact: Christiaan Schiepers, MD, PhD, Molecular and Medical Pharmacology, David Geffen School of Medicine, AR-144 CHS, 10833 Le Conte Ave., Los Angeles, CA 90095-6942. E-mail: cschiepers{at}mednet.ucla.edu

¹⁸F-FDG is in widespread use in cancer imaging but has limited utility in staging and monitoring of prostate cancer. 1-¹¹C-Labeled acetate, a substrate for the citric acid cycle, is superior. The kinetics of prostate tumors were investigated. Methods: Ten patients with primary prostate cancer, 10 with recurrent tumor, and 2 men with benign prostate hypertrophy were studied. After administration of 5.5 MBq/kg 1-¹¹C-acetate, dynamic PET of the pelvis was acquired for 20 min. Images were reconstructed with iterative algorithms, and corrections for attenuation and scatter were applied. Factor analysis produced factor images, representing iliac vessels and the prostate from which blood-input and tissue-output functions were derived with simple thresholding techniques. Five different kinetic models were applied to the dynamic data to estimate the rate constants. Results: The standard 3-compartment, 2-tissue model was able to describe 1-¹¹C-acetate kinetics of the prostate. The model could be reduced to 3 parameters by setting the tissue blood fraction and release from the second tissue compartment (k₄) to zero. Correction for metabolites appeared to be necessary. This reduced model performed marginally better than a 2-compartment model. A significant correlation was found between the influx rate constant (K) and acetate uptake (standardized uptake value) for primary tumors (r = 0.91), whereas there was no correlation for recurrent tumors (r = –0.17). Patlak graphical analysis provided accurate parameter estimates. Conclusion: A 3-compartment, 3-parameter model is able to describe adequately the acetate kinetics in prostate cancer. Significant differences between primary and recurrent cancer were found for transport k₁, influx K, distribution volume V_d, as well as early (6–10 min) and late (15–20 min) 1-¹¹C-acetate uptake.

Key Words: 1-¹¹C-acetate • PET • prostate cancer • benign prostate hypertrophy • kinetic modeling • factor analysis

COPYRIGHT © 2008 by the Society of Nuclear Medicine, Inc.

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