A B cell burden in prostate cancer
Although castration therapies such as androgen ablation are standard prostate cancer treatments, many patients develop resistance in 12-18 months.1 Now, researchers from the University of California, San Diego
and Scripps Florida have found that castration therapies themselves trigger an inflammatory response that could be partly responsible for such resistance. The findings make the case for complementing castration therapies with marketed biologics that can deplete B cells or block lymphotoxin signaling.
In a mouse model of prostate cancer, tumor cells killed by androgen deprivation released proinflammatory factors. This in turn led to infiltration by leukocytes, including B and T cells. A series of mouse allograft and genetic studies specifically implicated the B cells and the lymphotoxin they produced as