Cancer cells of all types have one thing in common: they have escaped the built-in controls of cell reproduction, and as a result, tumors grow as the out-of-control cells keep dividing.
This out-of-control cell division in cancer is very closely connected to a process called differentiation, the process by which a cell stops dividing and transforms itself from a stem cell into a specialized cell like a red blood cell. There is a trade-off: differentiated cells are specialized and tend to not divide; undifferentiated cells tend to divide but don't carry out specialized functions. The problem with cancer cells is that they are more like undifferentiated, dividing stem cells than the non-dividing, differentiated cells we want them to be.
In leukemia for example, you have cells in the blood that have failed to differentiate and failed to stop dividing. To treat leukemia, cancer researchers are interested in attacking both problems: they want to figure out how to get a cell to stop dividing and how to control the process of differentiation.
One of the key molecular players involved in controlling both differentiation and cell division is a protein called Myc. Mis-regulated Myc is a major problem in many cancers, but exactly how it works in cancer cells is still under investigation.
A group of researchers based at Cantabria University in Spain and Brown University have looked at how Myc controls the differentiation switch in leukemia cells. They found that Myc can prevent important blood cell differentiation genes from coming on in these leukemia cells, in part by blocking the activity of various transcription factor proteins that normally turn on the necessary genes for differentiation. Thus, if you could get around Myc and somehow activate these transcription factors, you might be able to treat some leukemias by inducing differentiation.
Myc is also interesting because it is one of four transcription factor proteins that researchers have used to turn skin cells into stem cells, which is essentially reverse differentiation - cells give up their specialization and regain the potential to turn into a different specialized cell. So Myc is clearly a potent controller of differentiation, and a critical target for cancer therapy. By understanding how Myc works, we can learn how to restore the normal function of out-of-whack control systems in tumor cells.
