Posted on October 29th, 2015 by
According to an international consortium of researchers led by experts at The Institute of Cancer Research, London, and The Royal Marsden, a pioneering drug developed to treat women with inherited cancers can also benefit men with advanced prostate cancer.
Olaparib, the world’s first drug to reach the market targeted against inherited cancer mutations, was found to benefit as many as a third of patients with prostate cancer, including many who did not inherit cancer genes but whose cancers had acquired defects in DNA repair. The results of this trial were released in the New England Journal of Medicine.
In the trial, 49 men with treatment-resistant, advanced prostate cancer received olaparib, and 16 of them (33%) responded, as defined by a set of clinical criteria. Olaparib stopped prostate cancer growth, generating lasting falls in prostate specific antigen (PSA) levels, falls in circulating tumour cell counts in the blood, and radiological responses on CT scans and MRI.
The clinical trial found that up to 30% of men with advanced prostate cancer had tumours with defects in their systems for repairing DNA detected by genomic testing – and that these responded particularly well to olaparib. Of the 16 patients with detectable DNA repair mutations, 14 responded very well to olaparib – accounting for the large majority of those who benefited from the drug. Most of these men, who all had terminal prostate cancer with limited treatment options, had disease control lasting much longer than expected in this group of patients.
The results have led to the start of TOPARP-B, a second part of this trial, in which only men whose prostate cancers have detectable DNA repair mutations will receive olaparib. If the results are successful, olaparib could become a standard treatment option for men with advanced prostate cancer and DNA repair mutations.
Reference: Mateo J, Carreira S, Sandhu S, et al. DNA-Repair Defects and Olaparib in Metastatic Prostate Cancer. The New England Journal of Medicine. 373:1697-1708. October 29, 2015.
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