Background and Objectives. To determine the most appropriate technique for tumour followup in experimental therapeutics, we compared ultrasound (US) and magnetic resonance imaging (MRI) to characterize ectopic and orthotopic colon carcinoma models. Methods. CT26 tumours were implanted subcutaneously (s.c.) in Balb/c mice for the ectopic model or into the caecum for the orthotopic model. Tumours were evaluated by histology, spectrofluorescence, MRI, and US. Results. Histology of CT26 tumour showed homogeneously dispersed cancer cells and blood vessels. The visualization of the vascular network using labelled albumin showed that CT26 tumours were highly vascularized and disorganized. MRI allowed high-resolution and accurate 3D tumour measurements and provided additional anatomical and functional information. Noninvasive US imaging allowed good delineation of tumours despite an hypoechogenic signal. Monitoring of tumour growth with US could be accomplished as early as 5 days after implantation with a shorter acquisition time (<5？min) compared to MRI. Conclusion. MRI and US afforded excellent noninvasive imaging techniques to accurately follow tumour growth of ectopic and orthotopic CT26 tumours. These two techniques can be appropriately used for tumour treatment followup, with a preference for US imaging, due to its short acquisition time and simplicity of use. 1. Introduction Colorectal cancer is the third leading cancer in the world in men and second in women with 1.2 million new cases identified in 2008. In terms of mortality, this cancer takes the second place after lung cancer with 608？700 deaths in 2008 [1]. It is therefore important to develop adapted models that could better represent the human pathology, in order to improve diagnostic methods or potential new therapies aimed at reducing the mortality rate of colon cancer. Murine colon tumour models can be obtained via in situ generation or via implantation of tumour fragments into appropriate syngeneic or immunosuppressed hosts. In situ models, including chemically induced, transgenic and spontaneous models, are considered less adapted for the evaluation of experimental therapies because of their inherent variability and the relatively long-time delay required for tumour growth and response to treatment [2]. While ectopic models are frequently employed owing to the ease of their implantation, orthotopic models are considered to better reflect the tumour physiological environment. In particular, significant differences between these models were found mainly in the level of growth factors and
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