Malignant tumors in transplant patients are generally attributed to a weakened immune system by medication. But a study in tomorrow's issue of Nature shows that drugs can play a more direct role: A common immunosuppressive can stimulate tumor cells to divide and spread. The conclusion suggests that it might be possible to design new drugs without the lethal side
For nearly 20 years, doctors have used cyclosporin to reduce the immune response, which would otherwise reject a transplant. - A strategy that carries with it an increase of 100 times the risk of tumors in these patients compared to healthy individuals. Recent experiments have shown, however, that cyclosporine may increase the body's production of TGF b , a growth factor known to promote tumor spread.
To further explore the role of cyclosporine in cancer, Minoru Hojo and colleagues from Tokyo University Medical School tested whether cyclosporine may help cancer cells become more mobile. They bathed a relatively mild strain of lung cancer cells in cyclosporine. Within 72 hours, the drugged cells began to extend pseudopods - appendages that help cell migration. Another experiment showed that the treated cells were in fact move more easily.
When the researchers injected these tumor cells into the tail veins of mice 35, almost twice sprouted new tumors in the lungs of cyclosporine treated mice compared to control animals. Exposed to cyclosporine, "tumor cells become smarter and more invasive" said Hojo. In experiments in both petri dish and the mouse, the effects of cyclosporine can be reversed by adding antibody against TGF b . for Hojo, this suggests that cyclosporine stimulates TGF b production in transplant patients, which in turn spurs cancer cells.
the discovery "sheds monkey wrench in our view of cyclosporine mechanism "for promoting tumor, says Gary Nabel, a molecular biologist at the University of Michigan, Ann Arbor. It can also force people to rethink the role of the immune system in cancer transplant patients, he said. the group of Hojo is now looking for ways to block TGF b 's tumor promoting capacity without reducing its effectiveness in reining in the immune system during transplant operations.
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