We are studying a specific set of proteins found to be working incorrectly, or not at all, in almost all human cancers.
Human cancers are deeply complex diseases. They arise from an accumulation of genetic mutations that interfere with the various processes through which cells are controlled. This can cause a loss of regulation that allows the affected cells to move and multiply in erratic ways. As further mutations emerge and proliferate, a specific instance of cancer becomes increasingly distinct, and can therefore be difficult to treat with current cancer therapies.
Despite these differences, different cancers still share remarkable underlying commonalities. Most mutations ultimately feed into a very specific shared set of core pathways and processes, although the amount they contribute can vary widely.
One of our principal interests is the enigmatic Myc protein, a master regulator of cell proliferation whose expression is mis-regulated in most, possibly all, cancers. The role of Myc is to coordinate the various processes involved in cell propagation throughout the body, particularly in tissues that are injured or still developing. Mis-regulation of Myc in cancers hijacks these physiological processes.
Another key interest is the p53 protein which works in contrast to Myc, like two opposing instruments in a duet, by restraining cell proliferation and helping to suppress cancers. p53 is inactivated by mutation in almost all adult human cancers. We study these shared cancer processes because, by targeting generalities, we hope to develop better, longer-lasting cancer therapies.