Saturday was never going to be a major day for prostate cancer at the annual meeting of the American Society for Clinical Oncology (ASCO) here in Chicago.
An early morning session included a number of papers dealing with potential future markers for prostate cancer risk and progression, but it has to be said that the data presented appears to be of very limited clinical significance at the present time.
- Ayala et al. discussed data suggesting that two clinical markers — the diameter of stromal tissue associated with perineural invasion and the extent and grade of reactive stromal tissue — may be predictive for more aggressive forms of prostate cancer in patients who had received a radical prostatectomy. However, what is critical to the best treatment of prostate cancer is to be able diagnose risk for more (and less) aggressive forms of disease prior to treatment, and there is no current means of assessing these two potential markers based on biopsy tissue.
- Cooney et al. presented information on genetic risk for early onset prostate cancer. They were able to show that men of < 56 years of age diagnosed with early onset prostate cancer carried more genetic risk alleles compared to either a control population or men diagnosed with prostate cancer at ≥ 56 yrs. Their data certainly demonstrate the potential to identify genetic variants when focusing on a sub-group of patients with early onset disease, but the practical application of such testing would be almost impossible because the number of men < 56 years of age with early onset prostate cancer is a very small proportion of the total population at risk.
- Third, Gallagher et al. explored the association between genetic markers and prostate cancer-specific mortality in 798 prostate cancer patients of Ashkenazi Jewish ancestry. They were able to identify two SNPs (single nucleotide polymorphisms) that were strongly associated with prostate cancer-specific survival and a third SNP strongly associated with risk for biochemical recurrence. However, this is again a very small subset of the overall prostate cancer risk community, and larger vstudies will be needed to validate the initial findings.
The “New” Prostate Cancer InfoLink appreciates the scientific interest of these studies, but has doubts about their long-term value in the ability to better manage the vast majority of newly diagnosed patients.
At the other end of the disease spectrum, at a session later in the day, Fizazi et al. presented data from a randomized, double-blind, multi-center, Phase III clinical trial comparing denosumab to zolendronate for the management of risk of skeletal-related events (including fractures) in men with metastatic, castration-resistant prostate cancer (mCRPC). The results of this study demonstrate that denosumab significantly delayed the time to a first on-study skeletal-related event compared with ZA. The median time to a first on-study skeletal-related event was 20.7 months for patients treated with denosumab compared with 17.1 months for the patients treated with zoledronate — a difference of 3.6 months. Denosumab also significantly delayed the time to first and subsequent on-study skeletal related events.
Zoledronate (Zometa) is the current standard form of therapy for prevention of skeletal-related events in patients treated with hormone therapy for advanced prostate cancer. If denosumab can consistently delay the onset of skeletal-related events (including fractures) in such patients by 3-4 months on average, then it is very likley that it will replace zoledronate at soem point in the future as the standard of care. However, that will only happen after the US Food and Drug Administration approves denosumab for this clinical use.