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This meeting report gives a short overview on the contributions of 17 leading scientists from China and Germany. The symposium was supported by the SinoGermany Science Center Bejing, the Deutsche Forschungsgemeinschaft and the National Science Foundation, China. It intended to foster communication and collaboration of researchers from both countries. The “Migrating Cancer Stem Cell”—Concept was discussed by Thomas Brabletz (Dept. of Surgery Univ. of Freiburg). Most colorectal adenocarcinomas (CRC) have mutations in the APC gene leading to overexpression of the Wnt-pathway effector beta-catenin. By acting as a transcriptional activator, nuclear beta-catenin is decisively involved in two fundamental processes in embryonic development: epithelial to mesenchymal transition (EMT) and generation of stem cells (e.g., in intestine development). We have previously shown that nuclear beta-catenin accumulates in tumor cells at the invasive front undergoing an EMT. The amount of these cells strongly correlates with clinical outcome and metastasis formation. In contrast, tumor cells in central tumor areas are differentiated and often show membranous, E-cadherin-bound beta-catenin. Strikingly, also, metastases show again a differentiated phenotype lacking nuclear beta-catenin, indicating a regulatory role of the tumor environment for malignant progression. Based on the developmental functions of beta-catenin and our data, we propose that both primary tumors and metastases are derived from the pool of EMT-associated “migrating cancer stem cells” at the tumor host interface, which are defined by strong nuclear beta-catenin accumulation and expression of its target genes. This gives these cells a feature, which drives malignant tumor progression including metastasis: The unusual combination of abilities allowing simultaneously to migrate and behave as a cancer stem cell. Molecular Targets in Cancer Therapy—New Possibilities and Old Limitations were reported by Reinhard Buettner (Inst. of Pathology, University of Bonn). Increasing knowledge on molecular pathogenesis of malignant tumors and activated signaling pathways has led to the concept of targeted therapies. Small molecularly designed molecules target specifically oncoproteins, and thereby modulate growth, apoptosis, or invasion of cancer cells. Currently, most experiences exit with membrane-coupled growth factor receptors and their intracellularly coupled signaling kinases. In cancer cells, these tyrosine kinase-triggered signaling pathways are frequently altered and causally involved in malignant transformation. Indeed, some of the tyrosine Virchows Arch (2007) 451:1099–1104 DOI 10.1007/s00428-007-0488-2

The first Sino-German symposium on cancer research, Shanghai May 2007