University of Cincinnati researchers have identified a specific cell receptor, which they say is a potential biological target for pancreatic cancer.
Led by Dr. Andrew Lowy and Dr. Susan Waltz, the study found that the RON receptor tyrosine kinase was "over-expressed" in pancreatic cancer cells, suggesting that the receptor may also contribute to the disease's development.
The researchers say that their findings, published in the journal Cancer Research, may help scientists better understand and treat the disease that kills more than 33,000 people each year.
Published in the journal Cancer Research, this is the first study to establish the link between the RON receptor and pancreatic cancer. The report also tells that receptor tyrosine kinases are proteins on the cell surface used to activate specific body functions like cell growth and migration.
"A normal pancreas has very low levels of RON, but our study showed that as tumours progress, so does the level of RON expression in the pancreas cells -- and those over expressed levels were maintained in 'metastases,' the areas that the tumours spread to," explains Waltz, Associate Professor and Director of the Oncology Research Program, Surgery Department, Cincinnati University.
During the study, the researchers noted that the RON receptor was active in 93 per cent of pancreatic intraepithelial neoplasia, an early form of pancreatic duct cancer. They also observed that the receptor was present in 79 per cent of primary pancreatic cancers, and 83 per cent of metastatic cancers.
Waltz believes that the RON receptor's signalling pathways may be a key factor contributing to pancreatic cancer progression, and that it may give drug developers a new target for RON directed therapies that are more effective in treating the deadly disease.
"When cells became invasive, we saw higher levels of RON expression that correlated with the aggressive nature of this disease and cancer metastasis. Clearly, this signaling pathway is associated with pancreatic cancer and merits further investigation," Waltz said.
During the study, the researchers used the protein HGFL to activate the RON receptor.
They observed that though stimulating the RON receptor had no effect on pancreatic cell growth, blocking it with targeted antibodies killed more cancer cells than did the standard treatment drug gemcitabine alone.
"Our findings suggest that combining antibodies that block the RON receptor and the standard chemotherapy drugs might stop progression of pancreatic cancer more effectively. RON could be a promising molecular target for future cancer drug development," says Waltz.
However, the researchers, who had reported in December last year the association between the RON receptor and breast cancer, say that further studies is needed before blockers for the RON receptors may be used for human testing.