The two views of malignancy, however, do not necessarily conflict. “It’s not as if accumulating mutations are at odds with the discernible program,” remarks Robert A. Weinberg of the Massachusetts Institute of Technology, noting that the activation of developmental programs could be a downstream consequence of the mutations. Weinberg showed last year that gene activity involved in maintaining embryonic stem cell identity is a common feature of the most undifferentiated-looking and aggressive tumors. Whether that kind of evidence indicates an embryonic program driving those cancers remains to be determined, he cautions: “It’s an interesting concept, but at this stage what they talk about is highly speculative. One can ascribe all manner of human traits to cancers and speculate that it will lead one into therapeutic insights. But the devil is in the details.”
Arresting Cancer’s Development
Evidence is growing that tumor cells may grow and spread by co-opting the genetic programs normally active only during embryonic and fetal development. If true, then disrupting those programs with gene-silencing therapy could undermine a tumor’s most threatening traits. Isaac S. Kohane of the Harvard-MIT Division of Health Sciences and Technology has organized cancers into three groups that correlate with different embryonic stages. He suggests that at the very least, drugs already known to work well on one cancer in his groupings should be tested against other cancers with the same profile.
This story was originally published with the title "Primal Programs"