Cancer biologists have lately come to appreciate the central role that evolution plays in the development of cancers. Yet just as oncology researchers have begun to incorporate solid evolutionary ideas into their understanding of cancer, a sea change in how we think evolution itself works is further transforming cancer biology.
It turns out that a lot of evolutionary change begins as temporary “epigenetic” modifications to the activity of genes without actually altering the genes themselves. Despite not being genetic, such epigenetic change can be passed from generation to generation in all sorts of living things.
No surprise then that cancer cells can perform the same trick. As I wrote for a feature in the current issue of Inside Stanford Medicine:
Decades of work had researchers convinced that cancer resulted from genetic mutations in individual cells. The theory was that a carcinogen, such as asbestos or cigarette smoke, induced mutations in a cell’s DNA that eventually caused it to become cancerous. That bad cell then multiplied and spread. But it has turned out that most of the things that cause cancer, including tobacco smoke and asbestos, don’t cause mutations.
Parag Mallick, PhD, a Stanford assistant professor of radiology, and a team of researchers are using the new understanding of cancer to build a virtual computer model of cancer that is expected to deliver useful and surprising answers to questions about cancer.
As Mallick told me: “Our goal is to build a computer program that you could come to with any protein and say, ‘OK, I’m interested in this protein and I’m looking at this cancer. Do you think it has potential to be a good biomarker?’”
Read more in my piece.
Photo of Parag Mallick by Norbert von der Groeben