Something Old Becomes Something New
We sometimes forget with all the modern painkillers out there, what a wonder drug good old aspirin is. The active chemical in aspirin is salicin, which was first extracted from Willow tree bark, and the modern form is the synthetic acetylsalicylic acid.
Aspirin began as a pain reliever as early as ancient Egypt and in 4000 BC when Hippocrates wrote about its use as a fever reducer. In the 1950s, people began taking it to prevent a heart attack or stroke for its blood thinning effect. Soon, it was prescribed to prevent a second cardiac event in those people, but that for some that can carry the risk of stomach bleeds.
The newest discovery of aspirin’s healing wonder is its role in cancer. It can prevent metastasis, or the spread of cancer, by stimulating a person’s immune response. What aspirin does is inhibit a chemical called cyclooxygenase which then inhibits the production of another chemical called thromboxane A two. That then allows for T cells that were already around a tumor site to respond more robustly.
Experiments showed that genetically modified mice had activated T cells at the tumor site which kept cancer cells from spreading to the liver and lungs. Aspirin essentially does the same thing through the reduction of thromboxane A two. For many years, aspirin has been called the “Wonder Drug” for its many benefits. With this new discovery, it may just be the MVP of drugs!
More Information
Researchers Find Possible Link Between Aspirin and Reduced Cancer Metastasis
A new study led by researchers at the University of Cambridge has revealed the mechanism behind how aspirin could reduce metastasis of some cancers by stimulating the immune system. The discovery may lead to the targeted use of aspirin to suppress the spread of susceptible cancers and aid the development of more effective drugs for preventing metastasis. The study was published in Nature.
Aspirin prevents metastasis by limiting platelet TXA2 suppression of T cell immunity
Metastasizing cancer cells are uniquely vulnerable to immune attack, as they are initially deprived of the immunosuppressive microenvironment found within established tumours3. There is interest in therapeutically exploiting this immune vulnerability to prevent recurrence in patients with early cancer at risk of metastasis. Here we show that inhibitors of cyclooxygenase 1 (COX-1), including aspirin, enhance immunity to cancer metastasis by releasing T cells from suppression by platelet-derived thromboxane A2 (TXA2).