Extraprostatic

Abstract: BACKGROUND A significant number of prostate adenocarcinoma patients undergoing radical prostatectomy are found to have microscopic extraprostatic disease extension. A majority of these patients have focal extraprostatic extension limited to one or both sides of the prostate. In addition, positive surgical margins are a common pathologic finding in this patient subgroup. In the current study, the authors evaluated the impact of positive surgical margins as an independent predictive factor for prostate specific antigen (PSA) progression in patients with pT3a/b N0M0 carcinoma. METHODS The Mayo Clinic prostate cancer registry list provided 1202 patients with pT3a/b NO prostate carcinoma (no seminal vesicle or regional lymph node involvement) who underwent a radical prostatectomy between 1987–1995. To reduce confounding variables, patients who received preoperative therapy or adjuvant therapy were excluded, resulting in 842 patients who were eligible for analysis. RESULTS A total of 354 patients (42%) had ≥ 1 positive surgical margins whereas 488 patients (58%) demonstrated no margin involvement. The sites of margin positivity were as follows: apex (n = 163), base (n = 47), posterior prostate (n = 227), and anterior prostate (n = 11). A total of 111 patients had ≥ 2 positive surgical margins. The 5-year survival free of clinical recurrence and/or biochemical failure (postoperative PSA level > 0.2 ng/mL) for patients with no positive surgical margins was 76% and was 65% for patients with 1 positive surgical margin (P = 0.0001). There was no significant difference in biochemical disease progression between patients with 1 versus those with ≥ 2 surgical margins (65% vs. 62%). Multivariate analysis revealed that positive surgical margins were a significant predictor (P = 0.0017) of clinical disease recurrence and biochemical failure (relative risk, 1.55; 95% confidence interval, 1.18–2.04) after controlling for preoperative PSA, Gleason score, and DNA ploidy. CONCLUSIONS In the current study, positive surgical margins were found to be a significant predictor of disease recurrence in patients with pT3a/b NO prostate carcinoma, a finding that is independent of PSA, Gleason score, and DNA ploidy. The benefit of adjuvant therapy in optimizing recurrence-free survival remains to be tested. Cancer 2002;95:1215–9. © 2002 American Cancer Society. DOI 10.1002/cncr.10871

Abstract: BACKGROUND This study was performed to identify clinical and histologic features most significant in predicting outcome in patients with transitional cell carcinoma (TCC) of the prostate without invasive bladder carcinoma. METHODS The histologic and clinical material from 50 patients with prostatic TCC without invasive bladder carcinoma were studied. The tumors were divided into the following locoregional categories: 1) TCC in situ (CIS) of the prostatic urethra; 2) CIS of the prostatic ducts and acini; 3) TCC with stromal invasion; 4) TCC with extraprostatic extension and/or seminal vesicle involvement; and 5) lymph node metastases. The Kaplan-Meier method was used to generate survival distributions for the locoregional categories, and comparison of survival curves was accomplished with the log rank test. RESULTS The 5-year disease specific survival rate was 52%. The 5-year disease specific survival rates for the locoregional categories were as follows: CIS of the prostatic urethra and prostatic ducts and acini (n = 19), 100%; TCC with stromal invasion (n = 21), 45%; TCC with extraprostatic extension and seminal vesicle involvement (n = 3), 0%; and lymph node metastases (n = 7), 30%. There was a significant difference in disease specific survival when patients with CIS were compared with patients with stromal invasion, extraprostatic extension and seminal vesicle involvement, and lymph node metastases (P = 0.0001). CONCLUSIONS This study demonstrates that patients with prostatic TCC involving prostatic stroma, extraprostatic tissues, seminal vesicles, and lymph nodes have a significantly poorer 5-year disease specific survival than patients with CIS. Cancer 1998;82:703-7. © 1998 American Cancer Society.