Pancreatic cancer is one of the most aggressive and deadly forms of cancer. It is often diagnosed at a late stage, when the disease has already spread to other organs such as the liver. Because of this, survival rates remain low, and scientists around the world are searching for new ways to slow the disease and improve treatment.
Now, researchers at the Indiana University Melvin and Bren Simon Comprehensive Cancer Center have discovered that a protein involved in blood clotting may play an important role in helping pancreatic cancer grow and spread.
Their study, published in the journal Gastroenterology, suggests that reducing levels of this protein could slow tumor growth and reduce the spread of cancer in the body.
The research was led by Dr. Melissa L. Fishel, an associate professor of pediatrics at the Indiana University School of Medicine and a Myles Brand Scholar in Cancer Research. Fishel is also a researcher at the Herman B Wells Center for Pediatric Research and co-leads the Cancer Biology and Microenvironment program at the cancer center.
The protein studied by the researchers is called fibrinogen. This protein is produced by the liver and plays an essential role in the body’s ability to stop bleeding. When the body is injured, fibrinogen is converted into another protein called fibrin, which forms a mesh-like structure that helps create blood clots and seal wounds.
While fibrinogen is vital for normal healing, researchers have begun to suspect that it may also influence how cancers grow.
Doctors have long known that people with pancreatic cancer often develop blood clots. In fact, patients with this disease have some of the highest rates of deep vein thrombosis, or DVT, which occurs when blood clots form in deep veins, usually in the legs. These clots can be dangerous and sometimes travel to the lungs.
Because of this connection, Fishel and her team wanted to understand whether the proteins involved in blood clotting were simply a side effect of pancreatic cancer or whether they might actually help the disease progress.
To investigate this question, the researchers focused on pancreatic ductal adenocarcinoma, often called PDAC. This is the most common form of pancreatic cancer and is known for its complex and dense tumor environment.
Unlike many other cancers, pancreatic tumors are surrounded by a thick network of cells and proteins. This environment, called the tumor microenvironment, includes special support cells known as cancer-associated fibroblasts. These fibroblasts produce a dense matrix of proteins that helps tumors grow and survive.
When the scientists examined healthy pancreas tissue, they found very little fibrin present. However, when they looked at pancreatic tumor samples, they found that fibrin was heavily deposited around the tumors.
This suggested that fibrin might play a role in shaping the environment where cancer cells grow.
To test this idea, the researchers conducted experiments using mouse models of pancreatic cancer. They used two different methods to reduce or remove fibrinogen in the mice. By lowering the amount of fibrinogen available, the researchers could study how the absence of fibrin affected tumor growth.
The results were striking. Mice with reduced fibrinogen developed significantly smaller pancreatic tumors compared with mice that had normal levels of the protein.
Even more importantly, the cancer spread much less often to the liver.
Pancreatic cancer frequently spreads to the liver in human patients, and once this happens the outlook for patients becomes much worse. The ability to reduce liver metastases therefore represents an important step toward improving outcomes.
Fishel explained that when fibrin was absent from the pancreatic tumors, the researchers observed a dramatic reduction in both the size of the main tumor and the number of cancer lesions that formed in the liver.
The team also wanted to understand whether fibrin circulating in the bloodstream contributed to the spread of cancer. To explore this, they used tumor models that allowed cancer cells to spread to organs such as the liver and lungs.
Interestingly, they found that the presence or absence of fibrinogen in the bloodstream did not significantly change the growth of metastatic tumors in those organs.
This suggests that fibrin’s most important role may occur at the original tumor site in the pancreas. According to the researchers, something about the absence of fibrin in the pancreatic tumor appears to change the behavior of cancer cells.
Without fibrin, the tumor cells may become less aggressive or less capable of leaving the pancreas and forming new tumors elsewhere in the body.
Although these findings are promising, the researchers stress that fibrinogen cannot simply be eliminated in patients. The protein is essential for blood clotting, and removing it completely could cause dangerous bleeding.
Instead, the goal would be to reduce fibrinogen levels to normal levels rather than removing it entirely.
Fishel explained that fibrinogen levels are often elevated in people with pancreatic cancer. If doctors could safely bring those levels back down to normal, it might help slow tumor growth while still allowing the body to form necessary blood clots.
The researchers emphasize that reducing fibrinogen alone is unlikely to cure pancreatic cancer. In the mouse experiments, lowering fibrinogen delayed the progression of the disease but did not completely eliminate the tumors.
Because of this, the team plans to explore combining fibrinogen-targeting approaches with existing treatments such as chemotherapy or newer therapies currently being developed for pancreatic cancer.
Understanding exactly how fibrin influences tumor cells will also be an important next step. Scientists hope to identify the signals and biological processes that fibrin activates inside tumors. By targeting those pathways, future treatments might become more effective.
The study was carried out as part of the Pancreatic Cancer Stromal Reprogramming Consortium, a national research collaboration focused on improving understanding of pancreatic cancer biology and developing better treatments.
The first author of the study was Dr. Nayela N. Chowdhury, a postdoctoral fellow at the Indiana University School of Medicine. Additional researchers involved in the study included Dana K. Mitchell, Silpa Gampala, Kylee Brewster, Wade Clapp, and Jia Wang.
Overall, the findings provide new insight into how the environment around pancreatic tumors can influence cancer growth. They also highlight the surprising role that blood clotting proteins may play in helping tumors develop and spread.
Although more research will be needed before these discoveries can lead to new treatments for patients, the results offer an encouraging new direction for scientists working to fight one of the most challenging cancers.
If you care about cancer, please read studies that artificial sweeteners are linked to higher cancer risk, and how drinking milk affects risks of heart disease and cancer.
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