%0 Journal Article %A Sandi Kwee %A Min-Ae Song %A Lenora Loo %A Iona Cheng %A Maarit Tiirikainen %T Chemotherapy associated changes in metastatic tumor 18F-fluorocholine uptake and circulating DNA levels in hormone-refractory prostate cancer %D 2011 %J Journal of Nuclear Medicine %P 1903-1903 %V 52 %N supplement 1 %X 1903 Objectives Cell-free DNA (cfDNA)from tumors may be found in the blood of cancer patients, although the actual source of these circulating nucleic acids may be difficult to localize. Because plasma cfDNA levels may increase as a result of chemotherapy-induced tumor lysis, we conducted a pilot study to explore the relationship between plasma cfDNA levels and changes in the metabolism of 18F-fluorocholine (FCH) by metastatic lesions identified on FCH PET/CT in patients receiving anti-microtubule chemotherapy for advanced metastatic prostate cancer. Methods Eight patients with hormone-refractory prostate cancer were recruited prior to receiving docetaxel-based chemotherapy. FCH PET/CT scans were performed at baseline and after the first treatment. Plasma cfDNA samples were collected on the day of each scan. Maximum standardized uptake values (SUVmax) corresponding to lesions identified on whole-body PET/CT were measured by region of interest analysis. Quantitative real-time PCR of genomic ALU repeats using a 115 base-pair amplicon was used to quantify cfDNA levels. Results At baseline, plasma cfDNA levels did not correlate with mean lesion SUVmax, net SUVmax, or total number of lesions identified on PET/CT. After the first dose of docetaxel, mean plasma cfDNA levels increased significantly from 13 ng/ml to 51 ng/ml (p<0.05). These changes in the plasma cfDNA concentration correlated with changes in mean lesion SUVmax (r=-0.77, p< 0.05). Conclusions Treatment with docetaxel is associated with a significant increase in plasma cfDNA levels in advanced metastatic prostate cancer. These changes in plasma cfDNA may be associated with changes in the FCH metabolism of metastases identified on PET/CT. Further research on FCH PET/CT as a predictor of chemotherapeutic response and method for identifying tumor sources of cfDNA are needed. Research Support This work is supported by NIH/NCI grant R21CA139687 and Queen Emma Research Foundation %U