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Evan Group - Peter Kreuzaler

Peter Kreuzaler

Position: Research Associate

Joined the lab: January 2012

Background: I studied Biochemistry at the Free University of Berlin, from where I graduated in 2007. I then moved to the University of Cambridge, where I carried out my PhD in the lab of Professor Christine Watson in the Department of Pathology. During my time in her lab, I studied the the mechanism of programmed cell death during post lactational mammary involution. We found that cells did not die via classic apoptosis, but rather via a novel type of programmed cell death that relies on large scale lysosomal membrane permeabilisation and the leakage of lysosomal proteases into the cytosol. This is the first major physiological event in mammals to be confirmed as being driven by a non-apoptotic type of cell death. I then moved on to the laboratory of Professor Gerard Evan, where I am using my knowledge of cell death to study the events that lead to tumour regression following inhibition of the oncogene Myc.

Current Projects: My current projects focus on understanding why tumour cells show an exquisite dependency on the Myc oncogene. I am focussing on models of myeloid leukaemia, in which I compare the effects of inhibiting all three Myc proteins (c-, L-.N-), as opposed to just c-Myc alone. This approach will give us insights into the continued need of Myc signalling, the overlapping activities of the different Myc proteins and most importantly, it will help us understand, which strategy to pursue for a pharmacological inhibition of Myc in tumours.

Interests: I play water polo at a competitive level.


    • Pensa, S., Neoh, K., Resemann, H.K., Kreuzaler, P.A., Abell, K., Clarke, N.J., Reinheckel, T., Kahn, C.R., and Watson, C.J. (2014). The PI3K regulatory subunits p55α and p50α regulate cell death in vivo. Cell Death Differ. 21, 1442–1450.
    • Kreuzaler, P., and Watson, C.J. (2012). Killing a cancer: what are the alternatives? Nature Reviews. Cancer 12, 411–424.
    • Littlewood, T.D., Kreuzaler, P., and Evan, G.I. (2012). All things to all people. Cell 151, 11–13.
    • Guzman, A., Zelman-Femiak, M., Boergermann, J.H., Paschkowsky, S., Kreuzaler, P.A., Fratzl, P., Harms, G.S., and Knaus, P. (2012). SMAD versus non-SMAD signaling is determined by lateral mobility of bone morphogenetic protein (BMP) receptors. The Journal of Biological Chemistry 287, 39492–39504.
    • Kreuzaler, P.A., Staniszewska, A.D., Li, W., Omidvar, N., Kedjouar, B., Turkson, J., Poli, V., Flavell, R.A., Clarkson, R.W., and Watson, C.J. (2011). Stat3 controls lysosomal-mediated cell death in vivo. Nat Cell Biol 13, 303–309.
    • Watson, C.J., and Kreuzaler, P.A. (2011). Remodeling mechanisms of the mammary gland during involution. The International Journal of Developmental Biology 55, 757–762.
    • Watson, C.J., and Kreuzaler, P.A. (2009). The role of cathepsins in involution and breast cancer. J Mammary Gland Biol Neoplasia 14, 171–179.