ust this early immune response, making it unnecessary to totally suppress the immune system when using this treatment.'
In the late 1990s, a student of Chiocca's discovered that the virus killed tumours more effectively when the animals were first given the drug. Chiocca then set out to learn why.
In this study, one of Chiocca's fellows, Giulia Fulci, now at Massachusetts General Hospital in Boston, examined brains from rats treated with the virus, with and without the drug to identify the immune cells present in the tumour before injection of the virus, and at different times afterward.
Six hours after the injection of the virus, she found that high numbers of NK cells, macrophages and brain-tissue immune cells called microglia had moved into the tumour. The number of macrophages, for example, had raised three fold. In animals given the drug, on the other hand, the number of these immune cells increased by only one half.
Other experiments performed together with Michael A. Caligiuri, director of the OSU Comprehensive Cancer Centre, revealed that when the drug is added to NK cells growing in the laboratory, the cells stop making an immune substance called interferon gamma (IFNg). One key effect of IFNg is to attract immune cells to an infection site. The production of the substance could therefore intensify the immune response against the anti-cancer virus.
Furthermore the researchers found that in rat brain tumours treated with the virus but not with the drug, IFNg levels rose by 10 times after six hours and by more than 120 times after 72 hours. Animals given the drug showed only small increases of IFNg.
Lastly, the researchers tested the treatment in brain tumours in mice that cannot make IFNg. They found that viral genes were expressed much more in these animals.
Overall, the study suggests that cyclophosphamide improves the cancer-killing ability of this virus by inhibiting the Page: 1 2 3 Related medicine news :1
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