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UID:595@biocityturku.fi
DTSTART;TZID=Europe/Helsinki:20240321T130000
DTEND;TZID=Europe/Helsinki:20240321T140000
DTSTAMP:20240311T091608Z
URL:https://biocityturku.fi/events/cellcom-seminar-brummer/
SUMMARY:CellCom Seminar\, Brummer
DESCRIPTION:March 21st at 13:00\nOn-site event\nÅbo Akademi seminar room\,
  BioCity\, A stairs\, 2nd floor\n\nCoffee\, tea and pastries will be serve
 d before the seminar\n\nProfessor Tilman Brummer\, Institute of Molecular 
 Medicine and Cell Research\, University of Freiburg\, Germany\nTowards mor
 e effective therapies for BRAF driven cancers – from molecular mechanism
 s to molecular tumour boards (and back)\n\nHost: Jukka Westermarck (jukwes
 @utu.fi)\n\n&nbsp\;\n\nTilman Brummer studied Biology at the University of
  Freiburg (UFR)\, Germany\, and conducted his PhD thesis on B lymphocyte s
 ignalling with Michael Reth at the Max-Planck-Institute for Immunobiology.
  This was followed by postdoctoral work on receptor tyrosine kinase signal
 ling in breast cancer in the laboratory of Roger Daly at the Garvan Instit
 ute of Medical Research in Sydney\, Australia. In 2008\, he established hi
 s 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 b
 y 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 Coll
 aborative Research Centre 1479 – OncoEscape\, investigating the interpla
 y between oncogenic signalling and immune escape mechanisms. He is also a 
 member of the Molecular Tumour Board at the Comprehensive Cancer Centre Fr
 eiburg (CCCF) and of the German Cancer Consortium (DKTK) in which co-initi
 ated the clinical trial SORATRAM.\n\nHis laboratory investigates the mecha
 nisms of oncogenic dysregulation of signalling pathways and their downstre
 am consequences on cellular phenotypes. The functional characterisation of
  novel tumour-associated mutations in signalling elements of the RAS/ERK p
 athway and the definition of their druggability represents another focus. 
 This work is carried out in close collaboration with Molecular Tumour Boar
 ds and a patient-derived organoid platform currently being established at 
 the CCCF.\n\n \n\nSelected publications\n\nLauinger\, 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.\, Forschn
 er\, A.\, Bitzer\, M.\, Wittel\, U. A.\, Boerries\, M.\, Ball\, C. R.\, He
 ining\, C.\, Glimm\, H.\, Frohlich\, M.\, Hubschmann\, D.\, Gallinger\, S.
 \, Fritsch\, R.\, Frohling\, S.\, O'Kane\, G. M.\, Dengjel\, J. &amp\; Bru
 mmer\, T. BRAFΔβ3-αC in-frame deletion mutants differ in their dimeriza
 tion propensity\, HSP90 dependence\, and druggability. Science Advances 9\
 , eade7486 (2023). https://doi.org:10.1126/sciadv.ade7486\n\nSpohr\, C.\, 
 Poggio\, T.\, Andrieux\, G.\, Schonberger\, K.\, Cabezas-Wallscheid\, N.\,
  Boerries\, M.\, Halbach\, S.\, Illert\, A. L. &amp\; Brummer\, T. Gab2 de
 ficiency prevents Flt3-ITD driven acute myeloid leukemia in vivo. Leukemia
  36\, 970-982 (2022). https://doi.org:10.1038/s41375-021-01490-0\n\nReisch
 mann\, N.\, Andrieux\, G.\, Griffin\, R.\, Reinheckel\, T.\, Boerries\, M.
  &amp\; Brummer\, T. BRAFV600E drives dedifferentiation in small intestina
 l and colonic organoids and cooperates with mutant p53 and Apc loss in tra
 nsformation. Oncogene 39\, 6053-6070 (2020). https://doi.org:10.1038/s4138
 8-020-01414-9\n\nHerr\, R.\, Halbach\, S.\, Heizmann\, M.\, Busch\, H.\, B
 oerries\, M. &amp\; 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:10.103
 8/s41388-017-0063-5
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CATEGORIES:Other events
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DTSTART:20231029T030000
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TZOFFSETTO:+0200
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