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Research focus

The research focuses of the institute are cell and tumor pathology, with emphasis on epithelia, epithelial tumors and the stroma. Here, questions concerning epithelial cell adhesion structures and mesenchymal cells of the normal and tumor stroma are addressed. Further research topics are new monoclonal antibodies against differentiation antigens and pathological questions in various interdisciplinary cooperation projects.

An important research focus is the glycoprotein CD34 expressed in a specific population of stromal fibrocytes.
Here, studies on the biology and pathology of CD34+ fibrocytes in two organs (urinary bladder and mamma) have been performed and several original and review papers have been published. In urinary bladder carcinoma, there is a fundamental phenotype change in stromal cells associated with a loss of CD34. This finding is likely to be important in local and systemic tumor spread. In contrast, in the invasive lobular type of breast carcinoma, CD34+ fibrocytes are often preserved. They may have prognostic significance in this tumor type, as their loss showed a correlation with the presence of lymph node metastases. CD34 was also used—together with CD141—as a marker for phenotypic characterization of endothelial cell types in the spleen.

Cell adhesion structures of epithelia and epithelial tumors, especially desmosomes, are another research interest of the institute.
The molecular components of desmosomes include the plakophilins (PKP 1 - 3), a family of proteins of the desmosomal plaque, some of which may also occur in the nucleus and, with respect to PKP 3, also in the cytoplasm. Our current questions are targeted at functions of the plakophilins outside the cell adhesion process. Here, several works on the interaction partners of PKP 3 were performed and specific and probably direct interactions with a translation initiation factor and a translation elongation factor as well as with a ribosomal protein were detected, indicating previously unknown roles of this plakophilin in protein synthesis. Another interaction partner (Ran) suggests a role for PKP 3 in mitosis. The transgenic mouse models we generated (PKP 3 knock-out) are being evaluated for phenotype.

Furthermore, several collaborative studies with research groups of the Institute of Molecular Biology and Tumor Research (IMT) of the Philipps-Universität Marburg, which also prepare a future participation of the institute in the Transregio-SFB 17, could be published. For example, increased tumor growth of transgenically induced mouse lung adenomas was demonstrated after silencing of a nuclear receptor gene of the PPAR family. For the ubiquitin-specific protease USP28, which is important for stabilization of the myc protooncogene, we demonstrated overexpression in colon and breast carcinomas.

In addition, the institute is involved in a variety of clinico-pathological collaborative projects. Among others, work on neuroendocrine tumors and thyroid carcinoma as well as cooperative studies with the anesthesiology and radiology departments have been completed.