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  Transcriptional regulation of tumor suppressor genes in colorectal tumorigenesis  
     
 
Colorectal cancer is one of the most frequent forms of cancer in Germany and also one of the most frequent causes of cancer-related death. As with other cancer types, mortality among colorectal cancer patients rises sharply with the occurrence of distant organ metastases. The formation of metastases is thought to occur in a stepwise process that is initiated when tumor cells begin to invade the surrounding tissue, detach from the primary tumor, disseminate via blood and lymphatic vessels, and eventually colonize a secondary organ.
 
 
Our research activities concentrate on the earliest steps of the metastasis cascade and the role of EPHB receptors in preventing tumor cell invasion. EPHB receptors are cell surface proteins that belong to the superfamily of receptor tyrosine kinases (Figure 1). They are activated through cell-cell contact-dependent interactions with EphrinB ligands on neighboring cells. In the healthy intestinal epithelium, EPHB/EphrinB signaling plays an essential role in the maintenance of tissue architecture by controlling the correct migration and positioning of stem cells, progenitors and their differentiated progeny. In colorectal cancer, EPHB receptors act as important tumor suppressors whose expression is frequently downregulated at the transcriptional level when tumors progress from the adenoma to the carcinoma stage.
 
     
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To understand how EPHB receptors contribute to the maintenance of epithelial cell characteristics and how tumor cells overcome the tumor suppressive function of EPHB receptors we apply cell biology, molecular genetics, genomics, proteomics and systems biology approaches. Of special interest are the Wnt/β-catenin and Notch signal transduction pathways, regulators of epithelial-mesenchymal transitions (EMT) and other factors with known functions in intestinal tissue homeostasis and colorectal tumorigenesis (Figure 1).
 
     
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