"What we think is going on is, when you kill the tumor, the body doesn't know it's the tumor being killed," Karin said. "It responds to it like there is tissue injury, a wound or something like that."
White blood cells called B-cells infiltrate the tumor and release a substance called lymphotoxin, a protein that kills infected cells. The research team found that exposure to lymphotoxin promoted the development of cancer cells resistant to hormone therapy. Interfering with the inflammatory response delayed the development of castration-resistant cancer.
"It's somewhat counterintuitive, that the death of these androgen-resistant cells somehow contributes to androgen resistance," said Dr. Durado Brooks, director of prostate and colorectal cancer for the American Cancer Society.
The finding could be key in developing a means to delay or stop the development of therapy-resistant secondary tumors. Until now, research into this resistance has focused on the role that the cells' androgen receptors play in the process. But researchers now can also consider controlling inflammation as another way to delay resistance.
Don't expect anything useful for humans anytime soon. Researchers will have to first make sure that human prostate cancer responds in the same way that the cancer did in mice.
"There's going to have to be a lot more work done to clarify that the mechanisms in humans are the same as those they have identified in mouse prostate cancer," Brooks said. "It's going to be quite a while before this mouse model moves to the bedside and actual clinical practice, if it ever does."
But if the findings do transfer to humans, this new understanding of the role of inflammation in prostate cancer treatment could help
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