TgAb plays a complementary role to Tg in the detection of recurrence of DTC. Tumour recurrence was more frequent in patients with elevated TgAb level over 140 U/ml or a trend toward increasing levels. PET/CT could provide additional information to I-WBS and neck USG in detecting tumour recurrence in patients with elevated TgAb.

The aim of this study was to investigate the feasibility of nuclear molecular imaging using the human sodium iodide symporter (hNIS) as a reporter gene to monitor macrophage migration toward the inflammatory foci. Methods: A stable macrophage cell line coexpressing hNIS and green fluorescent protein (GFP) genes (RAW264.7/hNIS-GFP and R NIS cell) was established from an immortalized macrophage cell line (RAW264.7 cells). 125 I uptake was determined (for hNIS protein functional activity), and flow cytometry analysis (to examine GFP gene expression), a cell proliferation assay, a cytokine assay, and a phagocytic activity assay were performed. 99m Tc-pertechnetate images were acquired at 1 d after subcutaneous inoculation of R NIS cells in nude mice. Chemical inflammation was induced for in vivo imaging in the thigh of nude mice by turpentine oil injection. Small-animal PET with 18 F-FDG and 124 I was performed with an intravenous administration of RAW264.7 or R NIS cells in inflammation-induced animals. Results: The expression of hNIS and GFP genes was confirmed in R NIS cells by flow cytometry and immunofluorescent staining. 125 I uptake was about 67 times higher in R NIS cells than in RAW264.7 cells. No significant difference was observed in cell proliferation, cytokine production, and phagocytic activity between RAW264.7 and R NIS cells. 99m Tc-pertechnetate imaging revealed increased tracer uptake at the inoculation site. PET with 124 I demonstrated a donut-shaped uptake, correlating with uptake shown by the 18 F-FDG PET images, at the inflammation site of mice administered R NIS cells. 124 I uptake (percentage injected dose per gram) was about 2.12 times higher at the inflammation site in the R NIS mice than in RAW264.7 mice. By immunohistochemistry, the migration of macrophages was further confirmed by positive staining for GFP and hNIS at the inflammation site of R NIS mice. Conclusion: These data support the feasibility of hNIS reporter gene imaging to monitor the macrophage migration toward an inflammatory lesion. Macrophages expressing hNIS may provide a new strategy to investigate the cellular behavior seen with inflammatory response in a preclinical model.

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