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The ability to measure tumor determinants of response to nucleoside analog (NA) chemotherapy agents such as gemcitabine and related compounds could significantly affect the management of several types of cancer. Previously we showed that the accumulation in tumors of the new PET tracer 1-(2'-deoxy-2'-(18)F-fluoro-β-d-arabinofuranosyl)cytosine ((18)F-FAC) is predictive of responses to gemcitabine. (18)F-FAC retention in cells requires deoxycytidine kinase (dCK), a rate-limiting enzyme in the deoxyribonucleoside salvage metabolism and in gemcitabine conversion from an inactive prodrug to a cytotoxic compound. The objectives of the current study were to determine whether (18)F-FAC tumor uptake is also influenced by cytidine deaminase (CDA), a determinant of resistance to gemcitabine; to develop a new PET assay using (18)F-FAC and the related probe 1-(2'-deoxy-2'-(18)F-fluoro-β-l-arabinofuranosyl)-5-methylcytosine (l-(18)F-FMAC) to profile tumor lesions for both dCK and CDA enzymatic activities; and to determine whether this PET assay can identify the most effective NA chemotherapy against tumors with differential expression of dCK and CDA.

the journal of nuclear medicine

Stratification of Nucleoside Analog Chemotherapy Using 1-(2′-Deoxy-2′-<sup>18</sup>F-Fluoro-β-d-Arabinofuranosyl)Cytosine and 1-(2′-Deoxy-2′-<sup>18</sup>F-Fluoro-β-l-Arabinofuranosyl)-5-Methylcytosine PET

Stratification of Nucleoside Analog Chemotherapy Using 1-(2′-Deoxy-2′-18F-Fluoro-β-d-Arabinofuranosyl)Cytosine and 1-(2′-Deoxy-2′-18F-Fluoro-β-l-Arabinofuranosyl)-5-Methylcytosine PET

Stratification of Nucleoside Analog Chemotherapy Using 1-(2′-Deoxy-2′-¹⁸F-Fluoro-β-d-Arabinofuranosyl)Cytosine and 1-(2′-Deoxy-2′-¹⁸F-Fluoro-β-l-Arabinofuranosyl)-5-Methylcytosine PET