Potential Target To Stop Breast-Cancer Metastasis Identified

Researchers at the University of North Carolina at Chapel Hill School of Medicine have found a potential target to stop the most deadly part of breast-cancer - metastasis.

In the study, Carol Otey, Ph.D. and UNC colleagues found that the ability of breast cancer cells to migrate could be reduced by knocking down the expression of a protein called palladin.

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They also found higher levels of palladin in four invasive breast cancer cell lines compared to four non-invasive cell lines.

"This study shows that palladin may play an important role in the metastasis of breast cancer cells as they move out of the tumour and into the blood vessels and lymphatics to spread throughout the body," said Otey, associate professor of cell and molecular physiology.

For the study, the researchers grew breast cancer cells in an 'invasion chamber,' in which human tumour cells are placed in a plastic well that is inserted into a larger well.

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Cells will try to move to the bottom of the chamber because it's baited with growth factors that cells find attractive.

However, first the cells have to migrate through a filter coated with a layer of artificial connective tissue.

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"The cells have to migrate through that and have to degrade it. It's a useful model system that mimics what happens in the body," Otey said.

Otey said that most women would never die from breast cancer if the cancer cells couldn't metastasize to the brain and bone marrow.

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"To really make breast cancer a treatable disease, we have to be able to find a way to prevent or reduce the amount of metastasis," Otey said.

"Now that we see palladin is expressed mostly in invasive cells, it raises the question as to whether it might be useful as a prognostic marker.

"Maybe someday doctors could test for the presence of palladin to identify patients who have the most aggressive tumours, then give those patients personalized, more aggressive treatment," Otey added.

The study appeared in the Nov. 3, 2008, online edition of the journal Oncogene.

Source-ANI
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