They found that this cross-talk weakens the ability of both cell types to fight off the cancer-fighting viruses.
The cells “talking” to the cancer cells are called cancer-associated fibroblasts (or CAFs). They are genetically normal cells that the cancer has conditioned to support the tumour. This conditioning makes the CAFs susceptible to virus infection, compared to their normal counterparts. In turn, the CAFs secrete a protein called FGF2 that makes the tumours more susceptible to virus infection.
Pancreatic cancer is among the deadliest of cancers, killing approximately 4,400 Canadians every year. Only 6% of people diagnosed with pancreatic cancer live longer than five years — a survival rate that has not improved in the last 40 years.
CAFs make tumours more resistant to standard therapies, and pancreatic cancers are known to have many CAFs. This study shows that this resistance does not apply, however, to cancer-fighting viruses. More CAFs and higher levels of FGF2 make tumours more susceptible to oncolytic virus therapy.
“Our findings could be important for patients in a couple of ways,” says study author Dr. John Bell, a senior scientist at the Ottawa Hospital Research Institute and professor of medicine at the University of Ottawa. “First, they could help us predict which cancer patients will be more likely to respond to oncolytic virus treatment.”
“More importantly, we saw improved outcomes in tumours treated with an oncolytic virus that expressed FGF2,” adds Bell, who is also scientific director of BioCanRx, a new network devoted to accelerating the journey of promising cancer biotherapeutic discoveries from the lab to clinical trials. “This, and the fact that the five-year survival rate for pancreatic cancer has been stuck in the single digits, motivates us to move this knowledge into clinical testing.”
For more information, please view the Ottawa Hospital Research Institute press release.
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Lois Ross, Senior Communications Specialist
Ottawa Hospital Research Institute
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