Researcher identifies function of GNAS mutation in evolution of pancreatic cyst into pancreatic cancer, establishing important biomarker identification and potential therapeutic target. 

Identifying a genetic mutation that affects fewer than one in 10 cancer patients may not sound monumental. That is unless you’re talking about pancreatic cancer, which kills 90% of patients within five years. 

“One of the biggest problems is that pancreatic cancer is detected very late stage, when it has already metastasized,” says Krushna Patra, PhD, University of Cincinnati Cancer Center member and assistant professor in the Department of Cancer Biology. “There are no early detection markers for pancreatic cancer, but there is a group of pancreatic cancers that develop from cysts that can be detected by imaging modalities.” 

Patra has been studying KRAS and GNAS mutations in pancreatic cancer and believes that the presence of these two mutations is a worrisome genetic makeup of precancerous cysts. While it is well-known that KRAS mutation is present in most pancreatic cancers, Patra’s lab is working on showing how the GNAS mutation is the conduit from cyst to cancer. The fact that this particular genetic mutation occurs in fewer than 10% of cases doesn’t deter him.  

“My work is understanding pancreatic cancer, one gene at a time,” Patra says. 

Currently, clinicians can analyze the fluid inside the cyst to detect the genetic mutation and based on this, determine if the cyst is precancerous and if it needs to be removed. However, because these cysts develop in elderly patients, surgery may not be feasible, or surgery may not remove all cancerous cells. Understanding how the GNAS mutation facilitates the growth of pancreatic cancer could lead to the first targeted therapy for pancreatic cancer.