摘要

We aimed to elucidate trans-1-amino-3-[F-18]fluorocyclobutanecarboxylic acid (anti-[F-18]FACBC) uptake mechanisms in inflammatory and tumor cells, in comparison with those of l-[methyl-C-11]methionine ([C-11]Met) and 2-deoxy-2-[F-18]fluoro-d-glucose ([F-18]FDG). %26lt;br%26gt;Using carbon-14-labeled tracers, in vitro time-course, pH dependence, and competitive inhibition uptake experiments were performed in rat inflammatory (T cells, B cells, granulocytes, macrophages), prostate cancer (MLLB2), and glioma (C6) cells. %26lt;br%26gt;Anti-[C-14]FACBC uptake ratios of T/B cells to tumor cells were comparable, while those of granulocytes/macrophages to tumor cells were lower than those for [C-14]FDG. Over half of anti-[C-14]FACBC uptake by T/B and tumor cells was mediated by Na+-dependent amino acid transporters (system ASC), whereas most [C-14]Met transport in all cells was mediated by Na+-independent carriers (system L). %26lt;br%26gt;The low anti-[F-18]FACBC accumulation in granulocytes/macrophages may be advantageous in discriminating inflamed regions from tumors. The significant anti-[F-18]FACBC uptake in T/B cells may cause false-positives in some cancer patients who undergo FACBC-positron emission tomography (PET).

  • 出版日期2014-6