on December 1st, 2015 No Comments
I’m constantly fascinated by the fact that the cells that make up a cancerous tumor are each undergoing their own private evolution every time they divide. Unlike most normal cells, cancer cells are so wacky that even a small batch can morph into a highly variable mass within a few generations. As I wrote in a story last week:
In many ways, cancer cells represent biology’s wild west. These cells divide rampantly in the absence of normal biological checkpoints, and, as a result, they mutate or even lose genes at much higher rate than normal. As errors accumulate in the genome, things go ever more haywire.
Recently, oncologist Hanlee Ji, MD, the senior associate director of the Stanford Genome Technology Center, and postdoctoral scholar Noemi Andor, PhD, devised a way to measure the extent of these differences among individual cancer cells and to associate their effect with the virulence of the disease as a whole. They published their results today in Nature Medicine.
As Ji, who is also a member of the Stanford Cancer Institute, explained in an email to me:
Until recently the scientific community believed that a typical tumor was composed of malignant cells with very similar genomes. The advent of next-generation sequencing technologies has revealed that this is not the case, and that most tumors are a heterogeneous product of ongoing evolution. This genetic heterogeneity also explains why therapeutic interventions in advanced cancers are often unsuccessful: some cells within a tumor develop resistance to therapies. Understanding the extent of tumor heterogeneity and how it leads to drug resistance is a major challenge in cancer biology research.