Blocking blood clotting could slow down cancer spread
Scientists in the US have found a way to slow down the spread of cancer by blocking blood cells called platelets - which drive the formation of blood cots in healthy people.
The vast majority of cancer deaths occur when cancer spreads from the initial tumour site by a process called metastasis.
In recent years, scientists have discovered that cancer cells appear to be aided in this process by platelets, which clump together and form a protective cloak around the cancer cells, protecting them against the body's immune response.
They also release substances called growth factors to help the cancer cells survive, and their ability to stick helps tumour cells to settle at a new site.
Now a team of researchers from Washington University School of Medicine in St Louis have tested the effect of two drugs that interfere with normal platelet function - aspirin and an experimental drug called APT102 - in mice with melanoma or breast cancer cells.
They found that the drug combination effectively reduced the number and size of 'secondary' breast cancers and melanomas in the bones of mice.
They also found that mice which had been given the drugs before being injected with cancer cells, and which then had additional treatments twice a day for two extra days, developed smaller and fewer tumours.
However, neither drug was effective on its own - an observation that the researchers attribute to the fact that tumour cells appear to be able to activate platelets in a number of different ways.
The drug combination did not cause seem to cause any abnormal bleeding, which can sometimes occur with platelet inhibitors.
Dr Katherine Weilbaecher, assistant professor of medicine and of cell biology and physiology, said: "Past research has shown that tumour cells activate platelets and that mice with defective platelets have significantly fewer metastases.
"We also know that platelets have several traits that can aid tumour cells, and we are working to break up that potentially lethal partnership."
Dr Weilbaecher revealed that aspirin works by preventing platelets from making a clotting protein, thromboxane, while APT102 "gets rid of a compound called ADP, which tumour cells release and which stimulates platelets to clump".
Ozge Uluckan, a predoctoral trainee in molecular genetics who also worked on the Journal of Cellular Biochemistry (JCB) study, revealed that the mice only received a small number of doses of the treatment.
"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.