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Aspirin May Prevent Cancer From Spreading, New Research Shows (scientificamerican.com)
An anonymous reader quotes a report from Scientific American: In recent years scientists have discovered another possible use for aspirin: stopping the spread of cancer cells in the body after an initial tumor has already formed. The research is still developing, but the findings hint that the drug could one day form the basis for a powerful addition to current cancer therapies. Not everyone responds equally well to the drug, however, and for some people it can be downright dangerous. Investigators are thus trying to develop genetic tests to determine who is most likely to benefit from long-term use of aspirin. The latest research into the drug's cancer-inhibiting activity is generating findings that could possibly guide those efforts. More recently, investigators have started to elucidate a third way that aspirin works -- one that interferes with the ability of cancer cells to spread, or metastasize, through the body. Intriguingly, in this case, the drug's anti-inflammatory properties do not appear to play the starring role. Researchers often inject tumor cells into the bloodstream of mice to approximate what happens during metastasis when cancer cells must navigate the bloodstream to find a new home in the body. When Elisabeth Battinelli, a hematologist at Brigham and Women's Hospital in Boston, and her team fed aspirin to certain strains of mice and then injected them with malignant cells, the investigators discovered that the platelets did not shield breakaway cancer cells from the immune system or produce the necessary growth factors that allow cancer cells to grow and divide in a new location. Thus, aspirin appears to fight cancer in two ways: its anti-inflammatory action prevents some tumors from forming, and its antiplatelet properties interfere with some cancer cells' ability to spread.
A big problem is that many "animal models" are wrong. For instance, we model Alzheimer's by using mice bred to reliably grow the beta amyloid plaques in brain tissue that are thought to cause the disease. We have developed dozens of drugs that prevent these plaques from forming in these mice. Yet, in human clinical trials NONE of these drugs has been effective. An obvious hypothesis is that the beta amyloids are just a symptom of Alzheimer's disease, and not the underlying cause. So the animal model may be completely wrong.