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Fluorescence tumor imaging using exogenous fluorescent tumor‐targeting agents has potential to improve early tumor detection. The fluorescent contrast agent indocyanine green ( ICG ) is used in medical diagnostics. The aim of the present study is to investigate the tumor imaging capability and the imaging mechanism of i.v. administered  ICG  in a mouse model of colitis‐associated colon cancer. To do this, an azoxymethane/dextran sodium sulfate‐induced colon cancer mouse model was used. Ex vivo imaging experiments were carried out 1 hour after i.v. injection of  ICG . The  ICG  fluorescence was observed in the colon tumor tissues, with sufficient tumor to normal tissue ratio, correlating with tumor malignancy. In the tumor tissues,  ICG  fluorescence was localized in the vascular interstitial tissue. Immunofluorescence microscopy revealed that tumor cells formed tight junctions normally, suggesting an inability of tumor cellular uptake of  ICG . In contrast, tumor tissues increased the  CD 31‐immunoreactive endothelial cell area, and accumulated stromal cells immunoreactive for  COX ‐2 and tumor cell population immunoreactive for inducible nitric oxide synthase. In vivo vascular permeability assay revealed that prostaglandin E 2  promoted the endothelial cell permeability of  ICG . In conclusion, our data indicated that fluorescence contrast‐enhanced imaging following i.v. administered  ICG  can be applied to the detection of colon tumors in a mouse colitis‐associated colon cancer model. The tumor tissue preference of  ICG  in the present model can be attributed to the enhanced vascular leakage of  ICG  involving inflammatory mediators, such as  COX ‐2 and inducible nitric oxide synthase, in conjunction with increased tumor vascularity.

Fluorescence tumor imaging by i.v. administered indocyanine green in a mouse model of colitis‐associated colon cancer