SAN FRANCISCO, Feb. 16 (Xinhua) -- Researchers have found that low-dose aspirin, or "baby" aspirin, may inhibit the normal function of blood platelets and reduce their ability to upregulate an "oncoprotein" called c-MYC, which plays an important role in cancer cell proliferation and survival.

The mechanism by which low-dose aspirin may have some benefits in helping cancer prevention, especially colon cancer, in addition to protection against cardiovascular disease, was the result of a study published in AJP-Cell Physiology by researchers at Oregon Health & Science University (OHSU) and Oregon State University (OSU).

"The benefit of aspirin may be due to its effect on blood cells called platelets, rather than acting directly on tumor cells," said senior author Owen McCarty, a professor in the Department of Biomedical Engineering at OHSU. "Our work suggests that the anti-cancer action of aspirin might be in part as follows: during their transit in the blood, circulating tumor cells interact with platelets, which spur tumor cell survival by activating oncoproteins such as c-MYC. The inhibition of platelets with aspirin therapy reduces this signaling between platelets and tumor cells, thus indirectly reducing tumor cell growth."

C-MYC orchestrates the expression of more than 15 percent of all genes, including those involved in cell cycles, survival, protein synthesis and cell metabolism.

However, it appears to be overexpressed in a large number of human cancers, including colon, pancreas, breast, lung and prostate cancers. "Early cancer cells live in what's actually a pretty hostile environment, where the immune system regularly attacks and attempts to eliminate them," said Craig Williams, a professor in the OSU/OHSU College of Pharmacy and co-author on the study. "Blood platelets can play a protective role for those early cancer cells and aid metastasis. Inhibition with aspirin appears to interfere with that process and c-MYC may explain part of that mechanism."

The study shows for the first time the ability of platelets to regulate the expression of the oncoprotein c-MYC in cancer cells.

Elevated expression of c-MYC has been found in almost one-third of colon cancers and 42 percent of advanced pancreatic cancer, the researchers wrote, concluding that "because the interaction between platelets and cancer cells is believed to occur early ... the use of anti-platelet doses of aspirin might serve as a safe and efficacious preventive measure for patients at risk for cancer."

Consistent with epidemiological studies which show that the anti-cancer benefit of aspirin occurs at very low doses, the researchers also found that the effect on platelet function is as great at low doses as it is at the higher doses, which are sometimes used to treat inflammation, headaches or pain, suggesting that clinicians will be able to use low doses of aspirin and minimize the risk of bleeding, which is a serious concern with any antiplatelet medication.

SAN FRANCISCO, Feb. 16 (Xinhua) -- Researchers have found that low-dose aspirin, or "baby" aspirin, may inhibit the normal function of blood platelets and reduce their ability to upregulate an "oncoprotein" called c-MYC, which plays an important role in cancer cell proliferation and survival.

The mechanism by which low-dose aspirin may have some benefits in helping cancer prevention, especially colon cancer, in addition to protection against cardiovascular disease, was the result of a study published in AJP-Cell Physiology by researchers at Oregon Health & Science University (OHSU) and Oregon State University (OSU).

"The benefit of aspirin may be due to its effect on blood cells called platelets, rather than acting directly on tumor cells," said senior author Owen McCarty, a professor in the Department of Biomedical Engineering at OHSU. "Our work suggests that the anti-cancer action of aspirin might be in part as follows: during their transit in the blood, circulating tumor cells interact with platelets, which spur tumor cell survival by activating oncoproteins such as c-MYC. The inhibition of platelets with aspirin therapy reduces this signaling between platelets and tumor cells, thus indirectly reducing tumor cell growth."

C-MYC orchestrates the expression of more than 15 percent of all genes, including those involved in cell cycles, survival, protein synthesis and cell metabolism.

However, it appears to be overexpressed in a large number of human cancers, including colon, pancreas, breast, lung and prostate cancers. "Early cancer cells live in what's actually a pretty hostile environment, where the immune system regularly attacks and attempts to eliminate them," said Craig Williams, a professor in the OSU/OHSU College of Pharmacy and co-author on the study. "Blood platelets can play a protective role for those early cancer cells and aid metastasis. Inhibition with aspirin appears to interfere with that process and c-MYC may explain part of that mechanism."

The study shows for the first time the ability of platelets to regulate the expression of the oncoprotein c-MYC in cancer cells.

Elevated expression of c-MYC has been found in almost one-third of colon cancers and 42 percent of advanced pancreatic cancer, the researchers wrote, concluding that "because the interaction between platelets and cancer cells is believed to occur early ... the use of anti-platelet doses of aspirin might serve as a safe and efficacious preventive measure for patients at risk for cancer."

Consistent with epidemiological studies which show that the anti-cancer benefit of aspirin occurs at very low doses, the researchers also found that the effect on platelet function is as great at low doses as it is at the higher doses, which are sometimes used to treat inflammation, headaches or pain, suggesting that clinicians will be able to use low doses of aspirin and minimize the risk of bleeding, which is a serious concern with any antiplatelet medication.