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A new hormonal treatment could soon give hope to prostate cancer suffers who have already undergone castration in an attempt to halt the spread of the disease.
The authors of the study, published in The Lancet, said that the agent, known as MDV3100, has shown encouraging anti-tumour activity against castration-resistant prostate cancer.
The phase one and two trial was carried out in five US centres in 140 patients with progressive, metastatic, castration-resistant prostate cancer and found MDV3100 was successful in reducing tumours even when they had become immune from the lower testosterone levels following castration.
Prostate tumours are dependent on testosterone for growth. Castration significantly reduces testosterone production, which kills many of the cancer cells and reduces the size of the tumour. However, those tumour cells that remain alive adapt to the low testosterone levels and regrow, at which point they are considered castration resistant.
But the new study has shown these cells do still respond the hormonal agents MDV3100, which works by blocking androgens from binding to the androgen receptor in tumour cells.
Using MDV3100 the study found there were anti-tumour effects at all doses, including decreases in serum prostate-specific antigen, which is a marker of prostate cancer, of 50% or more in 78 (56%) patients.
In addition, responses in soft tissue in 13 (22%) of 59 patients were recorded, stabilised bone disease in 61 (56%) of 109 patients, and conversion from unfavourable to favourable circulating tumour cell counts in 25 (49%) of 51 patients.
The most common serious adverse event was dose-dependent fatigue, in 16 or 11% of patients, which was mostly resolved after dose reduction.
The study leaders said: “We recorded encouraging anti-tumour activity with MDV3100 in patients with castration-resistant prostate cancer, both before and after chemotherapy. The results of this phase one and two trial validate in man preclinical studies implicating sustained androgen-receptor signalling as a driver in this disease.”
Copyright Press Association 2010
