CEACAMs were chosen for targeting as they are often GSI-IX highly expressed in a variety of malignancies. In order to broaden the specificity of our molecular probe, we used the T84.1 monoclonal antibody which is capable of recognising several members of the CEACAM family including CEACAM 1, 5 and 6. This contribution describes the expression of T84.1 immunoreactivity in 12 different human cancer cell lines for CEACAM expression in vitro and when grown in immunodeficient mice in vivo as primary tumour in order to establish a xenograft model for CEACAM detection. With one of these models we additionally investigated the accessibility of CEACAMs to antibodies in the primary tumour after i. v. application of the anti pan-CEACAM antibody T84.1. Identifying malignant tumours is one of the most important aims of molecular imaging. In order to bring molecular imaging techniques into clinical application, the technical approach has to be validated in suitable animal models first. We therefore systematically investigated the CEACAM expression of twelve human cancer cell lines and their primary tumour xenografts in immunodeficient mice for their suitability to detect the tumour using an anti CEACAM antibody as a pre-requisite for imaging studies. As human cancer cell lines often serve as the first choice for detecting human specific antigens, we analyzed CEACAM mRNA expression in a panel of human malignant cell lines. This was followed by the detection of their CEACAM protein expression in Western Blots. We found that pancreatic and colon cancer cell lines have the highest expression levels of CEACAM with good correlation between mRNA amount and protein level in Western Blots. Similarly high protein levels were detected in melanoma cells, but their mRNA level was generally lower than that observed in the pancreatic and colon cancer cell lines. This discrepancy between mRNA and protein expression levels has already been observed e.g. in Saccharomyces cerevisae for the PUP2, and by mammals for circadian Period2 gene. RNA stability and/or translational efficiency between the cancer cell lines and different CEACAM family members could be a reason for the finding, that low mRNA level were associated with high protein levels. A further discrepancy in CEACAM expression was observed between in vitro and in vivo CEACAM expression. Except melanomas, all malignant cell lines showed a downregulation of CEACAM expression in vivo as compared to in vitro. CEACAM family members are mainly expressed by epithelial and endothelial cells at the free surface of their apical pole. In contrast to the three dimensional growth in vivo where tumour cells form a 3D conglomerate of cells with only a few free surfaces, almost all cultured cells have exposed free surfaces and therefore almost all cells display an apical cell pole enabling them to express CEACAM at this interface to the cell culture medium. This different growth behaviour results in a down regulation of CEACAM in the primary tumours compared to the cell culture growth.