EAU15: Combination of pathology and research in prostate cancer

Sat, 21 Mar 2015

The Joint Meeting of the EAU Section of Uropathology (ESUP) and the EAU Section of Urological Research (ESUR) stressed the importance of combining pathology with morphology in modern medical practice and research.

The lectures underscored the need for continued research on high-risk and castration-resistant prostate cancer.

Prof. Dr. Sven Perner (DE) opened the session by describing the important role pathologists have in prostate cancer therapy. Prostate cancer is the most diagnosed cancer in men and although in most cases the disease develops slowly and patients die of comorbidities before the cancer is fatal, in a small group of patients the disease is very aggressive and deadly.

The question that keeps those involved in prostate cancer treatment and research on their toes is: “When cure is possible is it actually necessary and when cure is necessary is it still possible? Therefore, risk stratification of patients is essential and the role of the pathologist is important,” Perner said.

Despite the research that has been done to identify prognostic biomarkers, so far none are in use in the current clinical setting. Consequently, the Gleason score remains the key predictor for outcome and therapeutic choices and the pathological analysis of biopsies is crucial.

Dr. Anne Chauchereau (FR) discussed the issue of docetaxel resistance in patients with metastatic castration-resistant prostate cancer, which happens in about 50% of cases. Various elements of resistance have been studied but the molecular mechanisms are complex and, so far, there is no consensus on the definition of docetaxel resistance.

It is possible to bypass docetaxel resistance by using other therapies such as enzalutamide, abiraterone, radium223, or sipuleucel-T. None of these treatments are intended to overcome resistance.

Another option is to start treatment with the third-generation taxane cabazitaxel. Initial studies show that there is faster drug uptake and better intracellular retention time in cultured cells with cabazitaxel, but it is still unclear if the drug shares resistance mechanisms with docetaxel.

A third way is to inhibit the resistance mechanisms by identifying new relevant targets. In order to further develop this option it is necessary to decipher the mechanisms of docetaxel resistance.

Chauchereau: “There is an urgent need to set up new preclinical mouse models to evaluate the efficacy of new targets.