Credit: University of Missouri
In the fight against cancers, activating mutations in the RAS family of genes stand in the way of finding viable treatment options. Now, scientists at the University of Missouri and Yale University have discovered that one of these mutations -- oncogenic RAS or RASV12 -- is also responsible for the regrowth of cancer cells following genotoxic therapy treatment, or drugs that cause damage to a cancer cell's DNA in order to eliminate it from the body.
"Most of our knowledge of how cells respond to DNA damage is mainly derived from studies looking at the single cell level," said Yves Chabu, an assistant professor in the MU College of Arts and Science. "Therefore, we don't know much about how tumor cells respond to DNA damage in the broader context of the tissue level, and what possible implications these responses might have on a tumor's relapse following genotoxic therapies. To address this, we looked at how tissues containing patches of cells carrying oncogenic RAS mutations respond to DNA damage. We focused on oncogenic RAS because it is associated with cancers relapse and resistance to genotoxic therapies in humans. This approach has allowed us to identify novel cell-to-cell communication within the tissue that instructs tumor cells in tissues to regrow. It's something we would not have identified if we were only looking at the single cell level."