- Demonstrated essentiality of the serine/threonine kinase STK33 in mutant KRAS-driven cancer cells (Scholl, Fröhling et al. Cell 2009)
- Identified proteins that protect STK33 from degradation and provide new leads for the development of therapies attacking KRAS mutant cancers (Azoitei et al. J Exp Med 2012)
- Demonstrated that the leukemogenic transcription factor CDX2 inhibits the tumor suppressor KLF4 and causes deregulation of the PPARgamma signaling pathway, and that pharmacologic stimulation of the PPARgamma receptor induces KLF4 and results in differentiation and depletion of CDX2-positive AML cells (Faber et al. J Clin Invest 2013)
- Uncovered that MLL-rearranged acute myeloid leukemia cells are dependent on a non-redundant function of the cell cycle regulator CDK6 (Placke et al. Blood 2014)
- Described a distinct class of mutations in the serine/threonine kinase BRAF that possess intermediate biochemical activity, cooperate with mutant RAS to achieve an optimal level of MEK-ERK signaling, and represent potential therapeutic targets in various cancers (Kordes, Röring, Heining et al. Leukemia 2016)
- Identified the receptor tyrosine kinase FGFR1 as targetable oncogenic driver in multiple subtypes of soft-tissue sarcoma (Chudasama et al. Clin Cancer Res 2016)