Antigens, Neoplasm ; urine ; Antineoplastic Agents ; therapeutic use ; Biomarkers, Tumor ; blood ; urine ; Biopsy, Fine-Needle ; Brachytherapy ; Global Health ; Humans ; Male ; Prostate ; diagnostic imaging ; pathology ; Prostate-Specific Antigen ; blood ; Prostatectomy ; Prostatic Neoplasms ; diagnosis ; epidemiology ; therapy ; Radiotherapy ; Taxoids ; therapeutic use ; Ultrasonography

Robot-assisted radical prostatectomy (RARP) is a rapidly evolving technique for the treatment of localized prostate cancer. In the United States, over 65% of radical prostatectomies are robot-assisted, although the acceptance of this technology in Europe and the rest of the world has been somewhat slower. This article reviews the current literature on RARP with regard to oncological, continence and potency outcomes-the so-called 'trifecta'. Preliminary data appear to show an advantage of RARP over open prostatectomy, with reduced blood loss, decreased pain, early mobilization, shorter hospital stay and lower margin rates. Most studies show good postoperative continence and potency with RARP; however, this needs to be viewed in the context of the paucity of randomized data available in the literature. There is no definitive evidence to show an advantage over standard laparoscopy, but the fact that this technique has reached parity with laparoscopy within 5 years is encouraging. Finally, evolving techniques of single-port robotic prostatectomy, laser-guided robotics, catheter-free prostatectomy and image-guided robotics are discussed.
Erectile Dysfunction ; etiology ; Humans ; Male ; Prostatectomy ; adverse effects ; instrumentation ; methods ; Prostatic Neoplasms ; surgery ; Quality of Life ; Robotics ; methods ; Surgery, Computer-Assisted ; instrumentation ; methods ; Treatment Outcome ; Urinary Incontinence ; etiology

A cure cannot be assured for all men with clinically localized prostate cancer undergoing radical treatment. Molecular markers would be invaluable if they could improve the prediction of occult metastatic disease. This study was carried out to investigate the expression of BCL-2, Ki-67, p53 and E-cadherin in radical prostatectomy specimens. We sought to assess their ability to predict early biochemical relapse in a specific therapeutic setting. Eighty-two patients comprising 41 case pairs were matched for pathological stage, Gleason grade and preoperative prostate-specific antigen (PSA) concentration. One patient in each pair had biochemical recurrence (defined as PSA >or= 0.2 ng mL(-1) within 2 years of surgery) and the other remained biochemically free of disease (defined as undetectable PSA at least 3 years after surgery). Immunohistochemical analysis was performed to assess marker expression on four replicate tissue microarrays constructed with benign and malignant tissue from each radical prostatectomy specimen. Ki-67, p53 and BCL-2, but not E-cadherin, were significantly upregulated in prostate adenocarcinoma compared with benign prostate tissue (P < 0.01). However, no significant differences in expression of any of the markers were observed when comparing patients who developed early biochemical relapse with patients who had no biochemical recurrence. This study showed that expression of p53, BCL-2 and Ki-67 was upregulated in clinically localized prostate cancer compared with benign prostate tissue, with no alteration in E-cadherin expression. Biomarker upregulation had no prognostic value for biochemical recurrence after radical prostatectomy, even after considering pathological stage, whole tumour Gleason grade and preoperative serum PSA level.
Adenocarcinoma ; diagnosis ; metabolism ; surgery ; Aged ; Biomarkers, Tumor ; metabolism ; Cadherins ; genetics ; metabolism ; Case-Control Studies ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Ki-67 Antigen ; genetics ; metabolism ; Male ; Middle Aged ; Prognosis ; Prostate ; metabolism ; pathology ; Prostate-Specific Antigen ; blood ; Prostatectomy ; Prostatic Neoplasms ; diagnosis ; metabolism ; surgery ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; Risk Factors ; Tumor Suppressor Protein p53 ; genetics ; metabolism