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Prostate-specific membrane antigen (PSMA) is a 750 amino acid type II transmembrane glycoprotein expressed in normal human prostate epithelium.  However, PSMA is overexpressed on virtually all prostate cancer cells.  Poorly differentiated, metastatic and castration-resistant prostate cancers harbor even higher expression.  Hence, not only is PSMA a potentially good target for diagnostic imaging but also for targeted therapy.  The field of PSMA PET imaging offers significant promise and is currently being utilized for detection and may off potential to direct oligometastatic disease ablation. 
Just recently, we discussed the topic of neoadjuvant systemic therapy for cisplatin-ineligible patients with muscle-invasive urothelial carcinoma of the bladder.1  For those patients “unfit” for cisplatin with at least one of the following criteria: creatinine clearance <60 ml/min, grade ≥2 hearing loss, grade ≥2 neuropathy, ECOG performance status 2, and/or New York Heart Association Class III heart failure,2 there are no good options other than cystectomy alone.  Yet, we know the outcomes are not ideal for these patients with cystectomy alone.  Finding systemic therapies that may improve outcomes for these patients is clearly an unmet need in the field.
Three randomized phase 3 trials of adjuvant therapy for high-risk renal cell carcinoma have led to conflicting results.  S-TRAC was the one trial with a positive outcome, as sunitinib prolonged disease-free survival (DFS) by a median of 1.2 years compared with placebo (6.8 versus 5.6 years; HR 0.76, 95% CI 0.59-0.98, p=0.03).1  Based on these results, the US FDA approved sunitinib for the adjuvant treatment of patients with high-risk renal cell carcinoma.  However, the ASSURE trial revealed negative results as median DFS was 5.8 years for sunitinib, 6.2 years for sorafenib and 6.6 years for placebo.2  The PROTECT trial also had negative results as pazopanib compared to placebo had a HR 0.86; 95% CI
Although urothelial carcinoma of the bladder represents the fourth most common malignancy in men, 70% of these cases are non-muscle invasive (NMIBC).  Most of these patients will have outstanding outcomes, however, up to 70% will recur after initial treatment and 10-20% will progress to muscle-invasive bladder cancer (MIBC).1  Once a patient has MIBC, then treatment options become more intense, with discussions of definitive cystectomy, chemotherapy, and radiation, all of which carry greater morbidity and cost. 
We are now using PARP inhibitors for DNA repair-deficient patients with breast, ovarian, fallopian tube or primary peritoneal cancer.  In the realm of genitourinary oncology, we are meticulously exploring PARP inhibition, particularly for enriched patient populations with prostate cancer.  This is due to the fact that DNA repair deficiency occurs in approximately 23% of men with metastatic castration-resistant prostate cancer,1 and approximately 12% of men with metastatic prostate cancer harbor germline alterations.2
The title of this article is admittedly ironic and amusing. It goes back to the term “watchful waiting” of low and very low-risk prostate cancer. Although we were waiting for either something bad to happen or more often nothing exciting to happen due to indolent prostate cancer, the term “watchful” may have been a misnomer, as it is unclear if or how patients were being watched. The modern term of “active surveillance” is probably a more accurate term. It implies that patients are indeed, being surveyed by some accepted “active” script, usually with PSA testing and intermittent prostate needle biopsies. What that script looks like differs based on national
Antibody drug conjugates (ADCs) are a promising method of selective intensification of therapy, offering increased drug concentration to the target with minimal collateral damage to healthy tissue.1   Structurally, ADCs are monoclonal antibodies specific for a tumor antigen connected by a linker molecule to a cytotoxic drug payload.  After endocytotic internalization of the complex, the linker is degraded in a lysosome, releasing the cytotoxic payload.  There are now many FDA approved ADCs, including brentuximab vedotin for anaplastic2 and refractory Hodgkin lymphomas,3 trastuzumab emtansine

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