Selecting for Cancer

On the left, mice lung cancer cells are stained red. On the right, exosomes (labeled green) carry paclitaxel to the cancer cells. Image courtesy of UNC Eshelman School of Pharmacy.

Using evolution to explain the spread of cancer

In 2018, the International Agency for Research on Cancer estimated seventeen million new cancer diagnoses and 9.5 million cancer-related deaths worldwide. Though the numbers are grim, researchers have made great strides in explaining what causes and promotes cancer through an unexpected lens: evolution.

The Townsend Lab at the Yale School of Public Health has developed a model to predict the evolutionary progression of cancerous cells. Now, we can quantify the relative importance of different gene mutations in stimulating cancer growth–the so-called ‘cancer effect size’ of a gene. By applying evolutionary principles, scientists can help analyze what mutations are driven by natural selection in a cancer lineage. “Selection is what drives [cancer] once you get a mutation…[causing cells to] replicate more,” explained Professor Jeffrey Townsend.

Townsend and his team were able to calculate the mutation rate of cancer cells using tumor DNA sequencing. While some mutations may actually lead to cancer, others may have just happened to occur in those tumors. “If we see more [mutations] than expected by random mutation, then…it was more likely to lead to a tumor when you had those mutations in that gene,” Townsend said.

What does this mean for the future of cancer medicine? “The cure for various cancers will be therapies that manage to corner all of the evolutionary avenues of an evolving tumor and make it impossible for it to find a new way to grow,” Townsend said. Being able to determine the cancer effect size of gene mutations will provide insight into the development of cancer cells, and thus, improve treatments for cancer patients in the future.