She found that the B cells and both types of T cells in people with melanoma showed activity levels that differed from healthy people in only 25 of those genes. Seventeen of those 25 were normally turned on in response to interferon.
"Interferon normally acts as a critical signal in activating immune cells," said Critchley-Thorne. Without the ability to respond to interferon, those cells might detect the cancer but won't activate properly.
This type of experiment only shows that certain genes are turned on at different levels in people with melanoma. It doesn't prove that the cells behave differently than the immune cells of normal people. To verify that the interferon signaling was defective in people with melanoma, Critchley-Thorne isolated those cells and exposed them to interferon.
As predicted, immune cells from people with melanoma also failed to respond normally to the immune activation signal. However, she found that if she left the cells in the presence of a high dose of interferon for much longer than would normally be required, those cells did begin responding.
Lee said the finding explains why a common melanoma treatment, in which some doctors have treated patients with prolonged exposure to interferon, sometimes helps. "Doctors knew it worked in some people but didn't know why," Lee said. This data suggests that treatment works by overcoming the immune system's inability to react properly to interferon.
If Lee's suspicion turns out to be true, doctors may be able to screen melanoma patients for interferon response and provide prolonged interferon treatment for o
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Contact: Amy Adams
amyadams@stanford.edu
650-723-3900
Stanford University Medical Center
7-May-2007