March 21^st at 13:00
On-site event
Åbo Akademi seminar room, BioCity, A stairs, 2^nd floor

Coffee, tea and pastries will be served before the seminar

Professor Tilman Brummer, Institute of Molecular Medicine and Cell Research, University of Freiburg, Germany
Towards more effective therapies for BRAF driven cancers – from molecular mechanisms to molecular tumour boards (and back)

Host: Jukka Westermarck (jukwes@utu.fi)

Tilman Brummer studied Biology at the University of Freiburg (UFR), Germany, and conducted his PhD thesis on B lymphocyte signalling with Michael Reth at the Max-Planck-Institute for Immunobiology. This was followed by postdoctoral work on receptor tyrosine kinase signalling in breast cancer in the laboratory of Roger Daly at the Garvan Institute of Medical Research in Sydney, Australia. In 2008, he established his independent laboratory funded by the Emmy-Noether–Program of the German Research Foundation (DFG) at the Centre for Biological Signalling Studies BIOSS at UFR. In 2017, he was appointed as Full Professor of Medical Cell Research and Signal Transduction at the UFR, a professorship installed by the Heisenberg-Program of the DFG at the Institute of Molecular Medicine and Cell Research (IMMZ). He serves as co-director of the DFG funded Collaborative Research Centre 1479 – OncoEscape, investigating the interplay between oncogenic signalling and immune escape mechanisms. He is also a member of the Molecular Tumour Board at the Comprehensive Cancer Centre Freiburg (CCCF) and of the German Cancer Consortium (DKTK) in which co-initiated the clinical trial SORATRAM.

His laboratory investigates the mechanisms of oncogenic dysregulation of signalling pathways and their downstream consequences on cellular phenotypes. The functional characterisation of novel tumour-associated mutations in signalling elements of the RAS/ERK pathway and the definition of their druggability represents another focus. This work is carried out in close collaboration with Molecular Tumour Boards and a patient-derived organoid platform currently being established at the CCCF.

Selected publications

Lauinger, M., Christen, D., Klar, R. F. U., Roubaty, C., Heilig, C. E., Stumpe, M., Knox, J. J., Radulovich, N., Tamblyn, L., Xie, I. Y., Horak, P., Forschner, A., Bitzer, M., Wittel, U. A., Boerries, M., Ball, C. R., Heining, C., Glimm, H., Frohlich, M., Hubschmann, D., Gallinger, S., Fritsch, R., Frohling, S., O’Kane, G. M., Dengjel, J. & Brummer, T. BRAF^Δβ3-αC in-frame deletion mutants differ in their dimerization propensity, HSP90 dependence, and druggability. Science Advances 9, eade7486 (2023). https://doi.org:10.1126/sciadv.ade7486

Spohr, C., Poggio, T., Andrieux, G., Schonberger, K., Cabezas-Wallscheid, N., Boerries, M., Halbach, S., Illert, A. L. & Brummer, T. Gab2 deficiency prevents Flt3-ITD driven acute myeloid leukemia in vivo. Leukemia 36, 970-982 (2022). https://doi.org:10.1038/s41375-021-01490-0

Reischmann, N., Andrieux, G., Griffin, R., Reinheckel, T., Boerries, M. & Brummer, T. BRAF^V600E drives dedifferentiation in small intestinal and colonic organoids and cooperates with mutant p53 and Apc loss in transformation. Oncogene 39, 6053-6070 (2020). https://doi.org:10.1038/s41388-020-01414-9

Herr, R., Halbach, S., Heizmann, M., Busch, H., Boerries, M. & Brummer, T. BRAF inhibition upregulates a variety of receptor tyrosine kinases and their downstream effector Gab2 in colorectal cancer cell lines. Oncogene 37, 1576-1593 (2018). https://doi.org:10.1038/s41388-017-0063-5