Inhibiting Protein May Stop Spread of Pancreatic Cancer


Granulin implicated in the spread of cancer from the pancreas to the liver.

New findings on how pancreatic cancer spreads to the liver could be a key factor in stopping the spread of the disease.

Metastatic pancreatic ductal adenocarcinoma (PDAC) is an aggressive form of pancreatic cancer that kills 330,000 people a year, worldwide.

Since current treatments have little effect on PDAC, researchers chose to focus on the role stromal cells play in metastasis.

“A better understanding of the mechanisms underlying the metastatic spreading of pancreatic cancer is critical to improve treatment and patient outcome,” said lead study author Michael Schmid.

The majority of research over the last few years primarily focused on cancer cells, making it evident that non-malignant stromal cells and the formation of the tumor microenvironment has a strong influence on the course of cancer progression and metastasis.

During the current study, researchers discovered that stromal partners play a critical role in metastatic growth of the pancreatic cancer cells. Furthermore, the protein granulin, a key regulator of pancreatic cancer metastasis, was identified.

“Our work, which was a collaborative effort among several national and international research teams, provides evidence that pancreatic cancer metastasis critically depends on the support of stromal derived factors such as granulin and periostin, and that targeting these stromal factors may improve the outcome of this devastating disease,” Schmid said.

The results of the study reveal that the expression of inflammatory monocytes from granulin is a key factor in pancreatic cancer metastasis.

“These findings suggest the management or disruption of the secretion of this protein holds the key to stop cancer from spreading from the pancreas to the liver,” said researcher Sebastian Nielson.

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