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Deactivating Platelets may Inhibit Cancer Cell Progression

by VR Sreeraman on Mar 8 2008 5:28 PM

A new study at Washington University School of Medicine suggests that deactivating platelets, specialized blood cells involved in clotting, may inhibit cancer cell progression.

Cancer cells get a helping hand from platelets that shelter and feed tumour cells that stray into the bloodstream, making it easier for cancer to spread, or metastasise.

"Past research has shown that tumour cells activate platelets and that mice with defective platelets have significantly fewer metastases," said Dr Katherine Weilbaecher, assistant professor of medicine and of cell biology and physiology.

"We also know that platelets have several traits that can aid tumour cells, and we are working to break up that potentially lethal partnership," she added.

The team of researchers led by Weilbaecher examined the effect of two platelet inhibitors, aspirin and an experimental drug APT102 in mice injected with either melanoma or breast cancer cells.

The findings revealed that combination of two platelet inhibitors significantly decreased the number and size of breast cancer or melanoma tumours in the bones of the mice.

"We only had a small amount of APT102 to test, so in this set of experiments, we gave only a few doses of the drugs to the mice," said Ozge Uluckan, a predoctoral trainee in molecular genetics and co-researcher

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"At this point, we don't know if additional treatment would have further reduced the tumour burden, but it's clear that reducing platelet function had a positive result in this model of metastatic cancer," he added.

"Aspirin prevents platelets from making thromboxane, a substance that facilitates clotting," said Weilbaecher.

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"APT102 is an especially interesting drug because it gets rid of a compound called ADP, which tumour cells release and which stimulates platelets to clump. So APT102 prevents platelet activation in response to tumour cells," she said.

The study appears in advance online publication in the Journal of Cellular Biochemistry.

Source-ANI
SRM/L


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