Scientists discover killer protein which causes pancreatic cancer

Pancreatic cancer is one of the deadliest forms of cancer, with a survival rate of about 10%.
Sejal Sharma
Mouse pancreas cells with high levels of the protein SRSF1.
Mouse pancreas cells with high levels of the protein SRSF1.

Krainer lab/Cold Spring Harbor Laboratory 

Pancreatic cancer is possibly the deadliest form of cancer out there. Not easily diagnosed, pancreatic cancer starts to declare itself only once the cancer has reached its last stages. Treatment for cancer is limited, which is why the patient in almost all cases is given five years to live.

Research is slow and ongoing. Recently scientists developed a tiny device to deliver drugs directly to the pancreatic tumor, which in turn decreased the size of the cancer. Last year, another team of researchers discovered a molecule that targets and kills cancer cells.

While these are all impressive feats, there has been no definite cure for pancreatic cancer.

In another discovery that could bring us closer to early diagnosis, a team of researchers from the Cold Spring Harbor Laboratory (CSHL) in New York has been able to zero in on a protein that kick-starts and accelerates the formation of pancreatic tumors.

The team explored the role of RNA splicing, a genetic process that happens before protein production, in pancreatic cancer. The team found a protein called SRSF1, which helps regulate the process of RNA splicing. They found that high levels of SRSF1 caused inflammation, also known as pancreatitis.

The SRSF1 levels in the body must remain at a specific level and there’s a range of genes and proteins working together just to achieve that. But as it happens, due to numerous factors, this process can sometimes be irregular. This, unfortunately, causes inflammation, which often results in the formation of Pancreatic ductal adenocarcinoma (PDAC) tumors.

PDAC is not only the most highly aggressive type of cancer but also the most prevalent form of pancreatic cancer. Over 90 percent of its patients die within five years of their diagnosis.

The team of scientists conducted their study in an animal model. They found that when SRSF1 returned to normal levels, the organoids (small versions of tumors) stopped growing, said the press release.

CSHL Professor Adrian Krainer said, “PDAC is often found too late for treatments like chemotherapy and surgery to be very effective. But if we can clearly understand the underlying genetic mechanisms of PDAC, this might lead to earlier diagnoses and new types of therapies.”

Krainer said that there is still a lot of work to be done in order to explore the benefits of this research.

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