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Pancreatic cancer: A gene may be key to stopping the spread
- Pancreatic cancer is a severe cancer type that can be both aggressive and fatal.
- Experts continue researching new treatment options for pancreatic cancer, including ways to stop the spread.
- A new study found a mechanism that may be the key to slowing down the growth of pancreatic cancer, which may open up future treatment options.
Cancer can be a detrimental disease, and pancreatic cancer is one of the most severe types. Pancreatic cancer has a low five-year survival rate. It is often challenging to treat if surgery is not an option. Researchers are working to understand how pancreatic cancer works to develop more effective treatment methods.
A study published in Nature found that turning off the specific gene GREM1 results in a greater spread of pancreatic cancer. But turning the gene back on may lead to a reduced spread of pancreatic cancer. The discovery could lead to the development of pancreatic cancer treatments.
Pancreatic cancer: An immense impact
Pancreatic cancer is a severe type of cancer that impacts the pancreas. The pancreas is an organ that is essential to digestion and the body’s regulation of blood sugar. American Cancer Society notes that it can be difficult for medical professionals to find and diagnose pancreatic cancer early. Often people don’t have symptoms until after cancer has spread.
Pancreatic cancer has a low five-year survival rate of 11% at all stages. However, the five-year survival rate is around 42% when the tumor is still localized and hasn’t spread to other areas. Sometimes a surgical intervention can remove the tumor, and other times care is more supportive and focus on prolonging life.
Dr. Arif Kamal, the Chief Patient Officer with the American Cancer Society, explained to Medical News Today:
“Pancreas cancer is often diagnosed at later stages when symptoms of advanced cancer like weight loss, abdominal pain, or jaundice (yellowing of the eyes) appear. For most patients diagnosed, it is not curable and very serious. For those with earlier stages of pancreas cancer, surgery and radiation modalities with or without chemotherapy are options for management. For those with more advanced disease, typically, intensive chemotherapy for an indefinite period of time is prescribed.”
Because pancreatic cancer can be difficult to catch early and treat, one area of interest is how to keep pancreatic cancer from spreading to other organs.
GREM1 and pancreatic cancer
Researchers in this study examined the influence of a specific gene on the spread of pancreatic cancer. They used mice and organoids in their research. Organoids are synthetically grown and simplified organs.
They looked at the most common type of pancreatic cancer: pancreatic ductal adenocarcinoma (PDAC). As this cancer spreads, it transitions from a certain type called epithelial to another type called mesenchymal. This shift impacts the aggressiveness of pancreatic cancer and the effectiveness of medications.
They found that a specific gene, GREM1, was essential to keeping pancreatic cancer in the more stable epithelial state vs. the more dangerous mesenchymal state. They noted that among mice with pancreatic cancer, when they removed GREM1, cancer switched from the epithelial state to the mesenchymal state within days.
Researchers found that pancreatic cancer metastasized to the liver in 90% of mice with GREM1 removed. By comparison, liver metastasis was only seen in 15% of the mice with standard (“wild-type”) GREM1.
In contrast, when the mice overexpressed the GREM1 gene, cancer reverted to the epithelial state. The findings suggest that this gene plays a key role in regulating whether or not pancreatic cancer spreads to the rest of the body and becomes more dangerous.
Study author, Professor Axel Brehens, noted the highlights of the research findings to MNT:
The main message of our study is, in my view, that it is possible to convert an aggressive pancreatic cancer into a more treatable form. We have done this by switching on and off one particular gene, GREM1. Future research should identify drugs that are able to mimic what this protein does and convert the tumour into a less aggressive form, which then could be better treated.
Study limitations and continued research
The data researchers collected in this study is beneficial but not without its limits. For example, they used mouse models and organoids, so the data translation over to humans is limited. However, targeting this gene may be key in developing future treatments for patients with pancreatic cancer.
It will take time for this data to translate over to treatment options, but Dr. Kamal was optimistic.
“This study demonstrates the unique cells that make up pancreas cancer and add further information to our understanding of how possible variations can lead to better treatment regimens,” he said.
Due to the limited survival rate of pancreatic cancer, this study adds to a growing understanding of this cancer and its aggressive nature. As the information in this area grows, it will hopefully lead to greater survival rates among pancreatic cancer patients.
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