A study published in the Journal of Experimental Medicine on Monday revealed new research that showed pancreatic cancer metastasis may be suppressible by inhibiting a protein that regulates cell movement.
A study published in the Journal of Experimental Medicine on Monday revealed new research that showed pancreatic cancer metastasis may be suppressible by inhibiting a protein that regulates cell movement.
Researchers from the Sanford Burnham Prebys Medical Discovery Institute drew their conclusions by taking a closer look at pancreatic cancer cells, which grow quickly and sap nutrients from their environment. In pancreatic cancer metastasis, tumor cells are able to migrate to new parts of the body. Now, the scientists believe that the inhibition of a protein called Slug may be beneficial.
“Pancreatic cancer cells are notorious for their ability to escape from a tumor. Even when pancreatic cancer is caught early, tumor cells are already found circulating throughout the body,” said Cosimo Commisso, Ph.D., an associate professor in Sanford Burnham Prebys’ NCI-designated Cancer Center and senior study author. “Our study suggests that we may be able to create treatments that stop pancreatic cancer cells from untethering in the first place, which could reduce metastasis and help more people survive this deadly cancer.”
To conduct their research, the team used a mouse model of pancreatic cancer. In response to glutamine deficiency, Slug appeared to drive metastasis by activating the epithelial-mesenchymal transition (EMT), which is the process that cells use to free themselves from packed tissue. When the researchers inhibited Slug, there was a reduction in the number and size of secondary lung tumors in the mice.
The scientists were also able to draw the conclusion that higher levels of Slug within the body were linked to a poor prognosis.
“The field of pancreatic cancer research is still working to understand the role of EMT in metastasis. Our study shows that glutamine deficiency indeed activates EMT, through Slug, to allow pancreatic cancer cells to escape and look for nutrient-rich grounds,” says Maria Victoria Recouvreux, Ph.D., a staff scientist in the Commisso lab at Sanford Burnham Prebys and the first author of the study. “In addition to revealing new therapeutic avenues that may halt pancreatic cancer metastasis, these findings might also apply to other tumors that rapidly consume glutamine, including lung and colon cancers.”
As of late, progress has been made in the pancreatic cancer realm, with AstraZeneca and MSD Inc. (known as Merck & Co. inside the U.S. and Canada) announcing on June 1 that they had received marketing authorization in the European Union for one of their treatments. Olaparib, which is sold under the brand name Lynparza, is a first-line maintenance treatment for germline BRCA-mutated (gBRCAm) metastatic pancreatic cancer.
Lynparza is approved in the U.S. and other countries as a first-line maintenance treatment for gBRCAm metastatic pancreatic cancer based on data from the Phase 3 POLO trial. The randomized, double-blind, placebo-controlled trial looked at 300mg of Lynparza, twice per day, against a placebo. The primary endpoint was progression-free survival, while secondary endpoints included overall survival, time to second disease progression, overall response rate and health-related quality of life. Lynparza nearly doubled the time trial subjects lived without disease progression or death to a median of 7.4 months versus 3.8 months on the placebo.
“Patients with advanced pancreatic cancer have seen limited treatment advances over the last few decades,” said José Baselga, Executive Vice President, Oncology R&D, AstraZeneca. “We are now one step closer to bringing the first targeted medicine to certain biomarker-selected patients with advanced pancreatic cancer in the EU.”
