ASCO commentary and update no. 3


There were probably over 100 posters related to prostate cancer presented at the ASCO meeting today (Sunday, May 31), so you will have to pardon us for not even attempting to report on all this vast variety of data. Rather, we have attempted to select out the papers that seem to offer the most interesting and immediately valuable knowledge for the patient community.

This commentary and report covers papers presented at a poster session and a follow-up poster discussion session this morning.

Among the most interesting of these papers was a poster from Danila et al. (abstract no. 5048) indicating that abiraterone acetate does in fact work in patients who have been previously treated with ketoconazole — but it definitely doesn’t seem to work as well in these patients as it does in the ketoconazole-naive patients. Median time to disease progression in docetaxel-treated, ketoconazole-naive, castration-resistant prostate cancer (CRPC) patients (198 days) was exactly twice as long as in patients who were otherwise comparable but who had received ketoconazole treatment (99 days). It is for this reasons that Phase III clinical trials of abiraterone acetate are being conducted only in ketoconazole-naive patients.

Two other papers in the same session (abstracts 5046 and 5047) provided final data on Phase II trials of abiraterone acetate in chemotherapy-naive CRPC patients not exposed to ketoconazole and in docetaxel-pretreated CRPC patients. Both studies confirmed the prior potential of abiraterone acetate, and the first of the two Phase III clinical trials of this drus is already fully enrolled.

Drewnowska et al. (abstract 5054) reported results of a prospective, multi-center, community practice-based clinical trial of PCA3 as a test to better identify risk for prostate cancer following initial risk analysis with PSA and/or DRE. The study clearly showed the higher specificity of the PCA3 test compared to PSA, but the PSA test is clearly the more sensitive of the two. The question is going to be how to integrate PCA3 testing into the diagnostic algorithm in order to optimize the likelihood of finding clinicallty significant disease while minimizing unnecessary biopsies.

Another paper, by Ross et al. (abstract 5052), also addressed the issue of diagnostic specificity — in this case comparing the sensitivity and specificity of a blood-based RNA transcript test to PSA data. The test developed by Ross and his colleagues appears to have very high levels of specificity and sensitivity compared to PSA testing, and potentially could significantly limit the need for unncessaty biopsies, but this test still needs to be validated in large mult-center trials.

A whole raft of other posters presented in this session provided data on the activity of drugs like bevacizumab, toremifene, denosumab, docetatxel + samarium-153 lexidronam, ixabepilone, sagopilone, dasatinib, AT-101, CNTO328, and panobinostat in late-stage prostate cancer. There are therefore suggestive data regarding the potential of these agents for the future, but it has to be said that none of the data made public so far appear to provide a compelling reason to think that any of these therapies can radically change long-term survival of patients with later-stage disease.

Finally, ASCO has published a report entitled “New Research on Signal Transduction Pathways in Prostate Cancer Reveals Potential Clinical Implications.” This report covers presentations from a clinical science symposium on Saturday morning dealing with some “heavy science” issues in prostate cancer drug development that may be of interest to some readers.

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