A protein that confers a worse prognosis in bladder cancer when present in high levels may be regulated by androgens such as testosterone, suggesting a role for antiandrogen therapy in this disease, similar to that used in the treatment of prostate cancer.
Overexpression of the protein CD24 was already known to be associated with poor outcomes in urothelial carcinoma and to contribute to tumor growth and metastasis. In the latest research, Dan Theodorescu, MD, PhD, of the University of Colorado Cancer Center in Denver, and colleagues reported in Proceedings of the National Academy of Sciences of the United States of America that mice—particularly male mice—unable to produce CD24 had fewer primary bladder tumors and metastases than did mice with intact CD24 levels. In human tumor samples, higher rates of relapse and shorter disease-free survival were associated with higher CD24 levels, again especially in males.
Because these sex-specific findings implied androgen involvement, the investigators knocked down androgen receptors in human bladder cancer cell lines, and observed a corresponding drop in CD24 levels as well as reduced cell proliferation. When CD24 was added, cell proliferation resumed, regardless of androgen levels.
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“We hope the results of these studies show the rationale for clinical studies of antiandrogen therapies with bladder cancer, especially in those tumors that happen to test markedly high in CD24 expression,” remarked Theodorescu in a statement issued by the University of Colorado–Denver. “The next step is moving this promising therapy to clinical trials with human patients.”
