Abstract
Prostate cancer is the most common cancer in men, both in the USA and Europe. Although incurable, metastatic disease can often be controlled for years with anti-androgen therapy. Once the disease becomes castrate resistant, the median survival is 18 months. There is growing evidence that the immune system, and in particular cytokines, play an important role in prostate cancer immunosurveillance and progression. Here, we have undertaken a clinical investigation of the role of two closely related cytokines, IL-4 and IL-13 in prostate cancer. In the largest series studied to date, we show that serum IL-4, but not IL-13 is significantly elevated in castrate resistant, compared to androgen sensitive disease. Notably however, serum IL-4 levels are also raised in patients with benign prostatic disease. Analysis of benign and malignant prostate tissue demonstrates that the source of IL-4 is epithelial cells rather than infiltrating leukocytes. Together, our data are consistent with a dual role for IL-4 in prostate cancer development. In benign disease, our data add to the evidence that IL-4 serves a protective role. By contrast, the data support a direct role for IL-4 in the progression of prostate cancer from androgen responsive, to advanced castrate-resistant disease.
Highlights
Prostate cancer is the most common male cancer in the USA and Europe
These were distributed into the following groups: (i) Radically treatable group; (ii) Androgen-sensitive disease, defined as patients on anti-androgen therapy, with at least two documented drops in serum levels of prostate specific antigen (PSA, n = 29); (iii) Castrate resistant prostate cancer (CRPC) group, defined as patients receiving a lutenising hormone releasing hormone (LHRH) agonist and an anti-androgen with two documented rises in serum PSA (n = 30)
Serum levels of IL-4 are raised in patients with castrate resistant prostate cancer, when compared with patients with organ-confined radically treatable disease
Summary
Prostate cancer is the most common male cancer in the USA and Europe. The disease is curable with radical surgery or radiotherapy. While metastatic disease cannot be eradicated, it can often be controlled for years with anti-androgen therapy. Evolution to castrate resistance is inevitable and median survival is only 18 months. Greater understanding of the mechanisms that underlie disease progression are of clear interest. Growing evidence suggests that interleukin (IL)-4 may play an important role in this transition [1,2]
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