Our laboratory is interested in the molecular processes that underlie tumorigenesis, tumor progression and tumor maintenance. Cancers appear very different from the normal tissues from which they are presumably derived, and this has engendered the widely held contemporary view that cancers are the protracted end result of a bewildering complexity of molecular lesions that between them drive the formation of the equally complex neoplastic phenotype. However, appearances can be deceiving. We know that many oncogenes are highly pleiotropic –master” switches that modulate a wide variety of mechanistically diverse processes. Consequently, the apparent complexity of cancers may be instructed by a relatively simple, and hence therapeutically tractable, set of molecular lesions. Our overarching aim is to establish what such molecular lesions might be, what effects they have on specific cell types, alone and in combination, and how critical such lesions are not only to drive tumor formation but also to maintain an established tumor.
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Selected Publications
Christophorou, M., Martin-Zanca, D., Soucek, L. Lawlor, E.R., Brown-Swigart, L., Vershuren, E. and Evan, G. I. (2005) Temporal dissection of p53 function in vitro and in vivo. Nature Genetics.
Flores, I., Murphy, D.J., Brown Swigart, L., Knies, U. and Evan, G.I. (2004). Exploiting inherent differentiation to counteract c-Myc-driven keratinocyte proliferation in vivo. Oncogene 23:5923-30.
Soucek, L., and Evan, G. (2002). Myc - Is this the oncogene from Hell? Cancer Cell 1:406-8.
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