Some years ago, the Herrlich laboratory developed a mouse tumor model that permits to explore processes of metastasis formation. The base of the model was laid by a Harvard laboratory: Mice with a defect in one allele of the tumor suppressor gene Nf2 (neurofibromatosis type 2) developed spontaneously several types of cancer which were highly metastatic. For the FLI tumor model these mice were crossed such that they lacked the gene for CD44. The result was a reduction of the number of tumors and, above all, these tumors had a strongly reduced ability to metastasize. Several questions arose: e.g.
- Is CD44 in tumor cells or in the microenvironment in the tumor-bearing mice responsible for metastasis formation?
- Can CD44 mutants (subfunctions of CD44) reconstitute metastatic ability?
- Analysis of sub functions, e.g. rescue of performance of CD44-negative macrophages by introducing the C-terminal tail of CD44 – role in bacterial and viral infections
- Molecular mechanisms of co-receptor functions of CC44 splice variants
Other projects, tumor-related or generated by the analysis of TRIP6:
- Regulation of the proteolytic release of growth factors and cytokines
- Orientation of cell division of stem cells (collaboration with the Ploubidou Laboratory)
- Differentiation of choroid plexus in brain and of progenitor cells
Scientific Director Emeritus