Pancreatic cancer has one of the worst survival rates of any cancer with only around 1 in 20 people surviving for a decade or more after their diagnosis. In the UK, over 10,000 people are diagnosed with pancreatic cancer each year and only 1 in 4 will survive for more than a year. But now, thanks to the kindness and generosity of supporters like you, a recent discovery could offer new hope for the future.
The reason pancreatic cancer is so difficult to treat is that the tumors are often fibrotic, which means they develop extra connective tissue throughout the pancreas. This connective tissue aids the growth of pancreatic cancer and provides a protective barrier against drugs and the immune system.
This protective barrier is made up of a type of cell called a cancer-associated fibroblast (CAF), which interact with cancer cells to help them grow and survive. Thanks to your donations, researchers in the US have now discovered that a protein called Netrin-G1, previously thought to only be involved in the development of neurons in the brain, is also produced by CAFs and plays a major role in the development and growth of pancreatic cancer. Their findings demonstrate for the first time how the protein helps pancreatic cancer cells survive by protecting them from the immune system and supplying them with nutrients.
The research has also shown that an antibody that neutralizes Netrin-G1 was able to stunt the progression of pancreatic tumors in mice, demonstrating the potential of this new route to developing new drugs.
This discovery could prove to be the starting point for developing new treatments for a type of cancer that desperately needs them. It couldn't have happened without you.
Dr Edna Cukierman, Associate Professor at Fox Chase Cancer Center in Philadelphia and Co-Director of the Marvin and Concetta Greenberg Pancreatic Cancer Institute, who led the study, said of the breakthrough:
“We saw that many pancreatic cancer patients express Netrin-G1 and that these patients tend to survive for a shorter time. So, in the future, detection of Netrin-G1 could be used to help diagnose patients. We also believe that limiting Netrin-G1 function could provide the starting point for the design of new treatments in a type of cancer that is in dire need of effective therapies.
We next plan to continue investigating the biology behind Netrin-G1 expression in CAFs, figure out a practical way to detect it in patients, and partner with industry to design Netrin-G1 blocking drugs. This way we hope that targeting Netrin-G1 could serve, one day, to treat pancreatic cancer patients."
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