Nicholas John Dyson
My laboratory studies the mechanisms that limit cell proliferation in normal cells and the ways that these controls are eroded in cancer cells.
Our research focuses on the E2F transcription factor and the retinoblastoma tumor suppressor (RB). E2F controls the expression of a large number of target genes that are needed for cell proliferation. This transcriptional program is activated when normal cells are instructed to divide but it is deregulated in tumor cells, where it provides a cellular environment that is permissive for uncontrolled proliferation. pRB has multiple functions, but one of its most important roles is to limit the activity of E2F; as a result, most tumor cells select for changes that remove this control.
Our current goals are threefold. First, since pRB physically interacts with multiple proteins we are profiling these interactions and testing the idea that RB-family members link the local regulation of promoter regions with a more general organization of chromosome structure. Second, using screening approaches, we are learning how to selectively kill cells that lack RB function and have deregulated E2F activity. We want to obtain a comprehensive picture of the pathways and genes that impact E2F activity, and that affect E2F regulation by pRB. Third, we have taken advantage of the fact that Drosophila has a streamlined version of the mammalian RB/E2F families of proteins. We have used this simplified system to define the roles of individual components, and to carry out genetic screens for interacting pathways that are important in vivo.
Cancer Ctr., CNY Bldg.149, Rm. 7.330A
149 13th Street
Charlestown, MA 02129