[Quality of life after biochemical recurrence in patients with prostate cancer. How and how long do patients live after biochemical recurrence?]. / Calidad de vida después recidiva bioquímica en los pacientes con cáncer de próstata. ¿Cómo y cuánto viven los pacientes después de recidiva bioquímica?

Routine monitoring of PSA in patients with localized prostate cancer radically treated permits to identify those with biochemical recurrence only. Treatment options for biochemical failure include observation, surgery, radiotherapy alone or combined with hormonal therapy, brachytherapy, cryotherapy and hormone therapy exclusively. These treatments determine a specific pattern of changes (urinary function, bowel, sexual and hormonal) that can negatively impact the quality of life, so that the indication must be made in a judicious way and always in consonance with patient's expectations and preferences. Decisions on how and when to treat biochemical failure are complicated and the impact of salvage therapy on clinical outcome is unknown. Rates of prostate cancer control after salvage therapy with prostatectomy, brachytherapy or cryotherapy vary between 20-80% of cases according to selected patient characteristics. Because individuals with BF may be clinically asymptomatic for many years without treatment, it is essential that physicians and patients have a clear understanding of the potential impact of these on the quality of life.

Prostate cancer perspectives after chaarted: Optimizing treatment sequence.

Prostate cancer is the most frequent cancer amongst men. Until recently, only two therapeutic options, initial androgen-deprivation therapy in patients without castration-resistant prostate cancer, with addition of docetaxel when the disease becomes castration-resistant, were considered as standard. In the last years, new drugs (abiraterone, enzalutamide, Ra-223, Sipuleucel) have been developed for prostate cancer treatment with important advantages in safety and efficacy. Results from the recent Chaarted study, in patients that received docetaxel for the hormone sensitive disease, have contributed to change the initial treatment approach in metastatic prostate cancer, in order to adapt the best sequence for each patient. Those results have been supported by the Stampede trial. Stampede survival data showed not only a benefit in overall survival of adding docetaxel initially, but also a prolonged time to first skeletal related event. Now it is discussed in which setting the available drugs should be administered. This review article summarizes the treatment options for patients treated with docetaxel initially for hormone sensitive prostate cancer after developing progressive disease, and offers an algorithm proposal for treatment.

Enzalutamide: a new prostate cancer targeted therapy against the androgen receptor.

Enzalutamide (MDV3100), an androgen receptor-signalling inhibitor, represents the most recent compound added to the therapeutic armamentarium for the treatment of metastatic castration-resistant prostate cancer (mCRPC) who progressed to docetaxel. The anti-tumour activity and safety of enzalutamide has been demonstrated in a phase III clinical trial, showing a benefit in overall survival, which was the primary endpoint. There are no head-to-head studies comparing the different treatment options in this subset of patients. In this article, most relevant data published in the literature have been reviewed, with special attention to the therapeutic alternatives currently available for postdocexatel mCRPC patients, emphasising the mechanisms of action of the different drugs, efficacy and quality of life-related aspects.

Temsirolimus in renal cell carcinoma with sarcomatoid differentiation: a report of three cases.

Renal cell carcinoma (RCC) with sarcomatoid features has an aggressive course. There is no standard treatment for this histological subtype. Some authors have previously reported the use of chemotherapy, but the activity of new agents against renal carcinoma with sarcomatoid differentiation has to be formally evaluated. Temsirolimus, an inhibitor of the mammalian target or rapamycin, is active in RCC, including those tumors with non-clear histologies. We have tested the activity of this agent in three consecutive patients. A first patient showed a rapid progression, dying 2 months after the diagnosis. The second patient showed clinical improvement and a partial response to lung metastasis that was maintained for 14 months. The third patient is still alive, evaluated as stable disease after 7 months on temsirolimus. Importantly, toxicity was not a main issue during the use of temsirolimus and only grade 2 hyperglycemia, asthenia, hyperlipidemia, and pleural effusion were detected. Temsirolimus is a valid therapy in this subset of patients, with some lasting stabilizations and with manageable toxicity.