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In vitro and in vivo studies with [(18)F]fluorocholine on digestive tumoral cell lines and in an animal model of metastasized endocrine tumor.
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International audience. PURPOSE: The aim of this study was to investigate (a) in vitro the relationship between [(18)F]fluorocholine ([(18)F]FCH) uptake and cell growth in endocrine cell lines and (b) in vivo the uptake of [(18)F]FCH by tumoral sites in an animal model of metastasized endocrine tumor. METHODS: In vitro studies were conducted on three endocrine and two nonendocrine digestive tumoral cell lines. The proliferative ratio was estimated using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay. The uptake of [(18)F]FCH and that of [(18)F]fluorodeoxyglucose ([(18)F]FDG) were measured before and after cytotoxic therapy. [(18)F]FCH biodistribution was studied in nude mice and in an endocrine xenografted mice model. RESULTS: The [(18)F]FCH uptake in tumoral cell lines was related to their proliferative capacities as measured by the MTT assay in basal conditions. After cytotoxic therapy, the IC(50) values calculated with the [(18)F]FCH incorporation test were very close to those determined with the MTT assay. Biodistribution studies showed that [(18)F]FCH was predominantly concentrated in the liver and kidney of nude mice. In the STC-1 xenografted animal model, the uptake of [(18)F]FCH in the primary tumor was only 1.1%. On autoradiography and micro-positron emission tomography, there was no uptake of [(18)F]FCH in liver metastases but there was a significant uptake of [(18)F]FDG. CONCLUSIONS: In vitro studies suggested that the incorporation of [(18)F]FCH in endocrine tumor cell lines was related to their growth capacities; however, in vivo studies conducted in an endocrine xenografted animal model showed an uptake of [(18)F]FCH in hepatic metastases lower than that in normal liver cells. An influence of the microenvironment or a competition phenomenon for [(18)F]FCH uptake between normal liver and endocrine tumor cells cannot be excluded.
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