Ph.D., University of Zurich, 2001
Cancer modeling and treatment; Senescence and tumor progression; cancer visualization; PTEN regulation
The past thirty years have shown massive advances in understanding molecular cancer biology.Yet, for the vast majority of patients, the traditional approaches of surgery, radiation- or chemotherapy still represent the best hope for effective treatment. Our major problem is that we recognize cancer as a genetic disease, but do not know the nature and extent of genetic alterations that occur when our cells become cancerous, simply because we are not yet able to measure them. With tremendous advances in genome analysis and increased access to patient tumor samples we may soon be able to read the cancerous transition of genomes. But this
technological advance directly leads to the second major problem, the interpretation of all the genetic changes. Finally, it is not clear if understanding the mechanisms behind the disease will indeed lead to a cure.
Our major research focus is solving the interpretation problem. We therefore aim to generate the best models of cancer. Most recently, we have developed RapidCaP, the first mouse model for live visualization and sequencing of endogenous metastatic prostate cancer. With this system, we can validate spontaneous genetic alterations by introducing them up front into the model. We use RapidCaP together with clinicians to define the genetics of metastasis and therapy resistance, and to identify novel biomarkers for lethal prostate cancer.
Our second focus is to understand the cell biology of cancer initiation. We realized that partial loss of tumor suppressors (e.g. PTEN-haploinsufficiency) drives many cancers. Thus, we now define how tumor suppressors are activated, transported and degraded so we can interfere to restore or even maximize their output.
Please visit Lloyd's Lab home page.
Xiong, Q., Oviedo, H.V., Trotman, L.C., and Zador, A.M. 2012. PTEN regulation of local and long-range connections in mouse auditory cortex. J. Neurosci. 32: 1643–1652.
Lessard, L., Labbé, D.P., Deblois, G., Bégin, L.R., Hardy, S., Mes-Masson, A.M., Saad, F., Trotman, L.C., Giguère, V., and Tremblay, M.L. 2012. PTP1B is an androgen receptorregulated phosphatase that promotes the progression of prostate cancer. Cancer Res. 72: 1529–1537.
Howitt, J., Lackovic, J., Low, L.H., Naguib, A., Macintyre, A., Goh, C.P., Callaway, J.K., Hammond, V., Thomas, T., Dixon, M., Putz, U., Silke, J., Bartlett, P., Yang, B.,Kumar, S., *Trotman, L.C., and *Tan, S.S. 2012. Ndfip1 regulates nuclear Pten import in vivo to promote neuronal survival following cerebral ischemia. J. Cell Biol. 196: 29–36.
Chen, M., Pratt, C.P., Zeeman, M.E., Schultz, N., Taylor, B.S., O’Neill, A., Castillo-Martin, M., Nowak, D.G., Naguib, A., Grace, D.M., Murn, J., Navin, N., Atwal, G.S.,Sander, C., Gerald, W.L., Cordon-Cardo, C., Newton, A.C., Carver, B.S., and Trotman, L.C.2011. Identification of PHLPP1 as a tumor suppressor reveals the role of feedback activation in PTEN-mutant prostate cancer progression. Cancer Cell. 20: 173–186.
Trotman, L. 2008. Lloyd Trotman: of mice and men, cancer, and PTEN. Interviewed by Caitlin Sedwick.J. Cell Biol. 181: 402–403.