"We showed that even after the tumor has taken hold, the antibody can either cure the tumor or slow its growth and prevent metastasis," says Irving Weissman of the Stanford University School of Medicine in Palo Alto, California, talking to Science.
Although still a long way to go, the findings have shown a new approach to dealing with cancers and, for the first time, discovered a chemical that acts on a wide variety of cancers.
Here is how it works: cancer cells deceive the body's own protection services - the immune system - by displaying a 'flag' or a sign that basically says "do not attack me, I am a friend". Such markers are commonly used by other important cells in the body, like blood cells.
What Weissman and his Stanford colleagues did was to block this marker, called CD47, in cancerous cells by introducing an anti-body designed for just this purpose. Once the "do not attack" sign was hidden, the body's police converged on the cancer cells and destroyed it.
Weissman's earlier work was on leukemia (blood cancer) and lymphoma (cancer of some immune cells). But in the latest research, he shows that the same approach is successful for a wide variety of cancers.
"What we've shown is that CD47 isn't just important on leukemias and lymphomas," Weissman told Science. "It's on every single human primary tumor that we tested."
The research results have been published in the online journal Proceedings of the National Academy of Sciences on March 26.
The researchers first exposed tumor cells to macrophages, a type of immune cell, in lab dishes. The macrophages ignored the cancerous cells. But when the anti-CD47 was introduced, the macrophages engulfed and destroyed cancer cells.
Next, similar experiments were done by transplanting human cancer cells into mice feet, where tumors can be easily monitored. When treated, the tumors shrank and did not spread to the rest of the body.
One problem was that presence of the anti-CD47 blocked the "don't attack" flags not only from targeted cancer cells but also from healthy blood cells. This led the macrophages to start attacking them. However, the researchers found that the decrease in blood cells was short-lived and the animals turned up production of new blood cells to replace those they lost from the treatment.
Apart from human testing, the new drug will also need to function in the complex, living micro-environment in a human body, which will be much different from the transplanted tumors in mice.
Weissman's team has received a $20 million grant from the California Institute for Regenerative Medicine to move the findings from mouse studies to human safety tests, Science reported.
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