Benign Glandular Tissue Research Articles

Pathological and Surgical Outcomes of Retropubic Radical Prostatectomy in an Academic Center: A Contemporary Study

Purpose: To report the peri-operative, pathological and oncological outcomes of a contemporary series of open retropubic radical prostatectomy (RRP), performed by one experienced surgeon on RRP technique developed by Barré C. Methods: We analyzed data of consecutive patients who underwent an RRP as first-line treatment for localized prostate cancer, from January 2014 to December 2018, in single French academic center. a) Benign capsular incision (BCI) and b) Benign glandular tissue incision (BGTI) were defined as: presence of inadvertent intraprostatic incisions into benign glandular tissue in regions where capsule was a) present and b) absent. Results: Overall, 312 patients were included. The rates of pT1c, pT2 and pT3 were 0.3% (n=1), 49.0% (n=153) and 50.6% (n=158), respectively. The rates of non-nerve sparing surgery (NSS), unilateral NSS and bilateral NSS were 20.5% (n=64), 31.4% (n=98) and 48.1% (n=150). The median length of hospital stay was 4.0 (3.0-5.0) days and the median estimated blood loss was 250.0 (150.0-180.0) milliliters. The total positive surgical margin (PSM) rate was 11.9% (n=37). The total pT2 PSM and pT3 PSM rates were 0% and 23.4% (n=37) and achieved a statistical difference (p<0.001). The total BCI and BGTI rates were 1.6% and 9.0 %. Biochemical recurrence occurred in 29 (9.3%) patients at median 1.0-year of follow-up. Conclusion: Retropubic radical prostatectomy performed as previously described by Barré C., is reproductible and ensures optimal surgical results, in a predominantly population of intermediate-risk prostate cancer and high-risk prostate cancer.

Abstract 445: Coordinate loss of CHD1 and MAP3K7 promotes aggressive prostate cancer

Abstract The genomic complexity of prostate cancer contributes to disease progression, resistance to therapy, and development of metastases. The genes CHD1 and MAP3K7 are signficantly co-deleted in 10-15% of primary tumors and combined loss of CHD1 and MAP3K7 expression is associated with poor disease-free survival. We recently validated MAP3K7 as a prostate tumor suppressor, but CHD1's role in prostate tumorigenesis has not been evaluated. In this study, we used a mouse prostate epithelial stem cell (PrP/SC) model and a human prostate cancer cell line (LNCaP) model to investigate how loss of CHD1 alone or in combination with MAP3K7 suppression affects prostate tumorigenesis. Suppression of Map3k7 increased proliferation of PrP/SCs. Chd1 suppression decreased growth of wildtype PrP/SCs but not PrP/SCs already deficient in Map3k7 expression. Similarly, suppression of CHD1 in LNCaP cells decreased proliferation when MAP3K7 expression was present, but not when MAP3K7 was suppressed. These data suggest that loss of CHD1 alone is deleterious to growth, but that MAP3K7 suppression can compensate for this growth inhibition. Chd1 and Map3k7-deficient PrP/SCs were then evaluated in vivo using tissue recombination. When Chd1-deficient PrP/SCs were recombined with fetal rat urogenital mesenchyme (rUGM) and implanted under the renal capsules of immunocompromised mice, grafts contained mostly benign glandular tissue with focal areas of mild hyperplasia/prostatic intraepithelial neoplasia (PIN). A few nuclear abnormalities were observed. Map3k7-deficient recombinants generated a mixture of benign tissue, PIN, and adenocarcinoma (consistent with our previous findings). The nuclear morphology of these grafts was unremarkable. Strikingly, dual Chd1-Map3k7 knockdown recombinants displayed massive glandular atypia with glands completely filled with AR-negative and p63-negative cells. These cells had large nuclei, prominent nucleoli, and abundant cytoplasm. Tumorigenicity of CHD1 and/or MAP3K7-deficient LNCaP cells was also assessed by subcutaneous implantation of cells into immunocompromised mice. Mice implanted with CHD1-deficient xenografts formed smaller tumors and had increased survival relative to mice injected with control LNCaP cells (p=0.0083). MAP3K7-deficient xenografts were similar in size and in survival rate compared to control LNCAP cells. Dual CHD1-MAP3K7 deficient xenografts, in contrast, showed increased tumor growth and decreased survival relative to control (p=0.0242), MAP3K7 alone (p=0.0462) and CHD1 alone (p=0.0002). Collectively, these data suggest that loss of CHD1 alone is anti-tumorigenic but that combined loss of CHD1 and MAP3K7 drives aggressive prostate cancer development. Citation Format: Lindsey Ulkus, Leah Rider, Cera Nieto, Lina Romero, Haitao Chen, Massimo Loda, Wennuan Liu, Jianfeng Xu, Scott Cramer. Coordinate loss of CHD1 and MAP3K7 promotes aggressive prostate cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 445. doi:10.1158/1538-7445.AM2014-445

Assessing the extirpative quality of a radical prostatectomy technique: categorisation and mapping of technical errors

To examine the extirpative quality of an open radical prostatectomy (RP) technique by first categorising and mapping all intraprostatic incisions into benign tissue and then determining a cumulative technical error rate given by all intraprostatic incisions into benign and malignant tissue. We performed a retrospective review of prospectively collected data relating to 1065 men with clinically localised prostate cancer who underwent open retropubic RP (70.6% nerve-sparing surgery [NSS]) by a single surgeon (January 2005 to December 2011). We recorded all intraprostatic incisions: (i) iatrogenic positive surgical margins (PSMs), (ii) deep or superficial benign capsular incisions (BCIs), (iii) incisions into benign prostate glands at the prostate apex or bladder neck (benign glandular tissue incisions [BGTIs]), and determined incision location, length and nature (solitary/multiple). We evaluated: (i) associations between benign incisions, NSS and PSMs, (ii) significant predictors for PSM risk by multivariate analysis, (iii) postoperative biochemical recurrence (BCR)-free survival (Kaplan-Meier method). Intraprostatic incision rates were 2.3% pT2 PSMs, 6.0% BCIs and 5.4% BGTIs. There were slight variations in rate over time and with NSS technique. Benign incisions were located as follows: 46.8% right posterolateral, 37.5% left posterolateral, and 15.7% bilateral for BCIs; 58.6% bladder neck and 41.4% apical for BGTIs. The median (range) incision length, for solitary and multiple incisions respectively, was 4 (1-13) and 9 (2-25) mm for BCIs and 1 (1-5) and 2 (2-6) mm for BGTIs. BCI rate, but not BGTI rate, was significantly associated with NSS (P = 0.004) and PSM (P = 0.005), and increased PSM risk 3.6-fold. A PSM increased BCR risk two-fold (odds ratio 2.078, 95% confidence interval 1.383-3.122). BCR-free survival decreased significantly even for short PSMs (<1 mm; P < 0.001). Although the pT2 PSM rate was low (2.3%), the cumulative technical error rate (patients with at least one pT2 PSM, BCI or BGTI) was five-fold higher (12.5%). Categorising and mapping intraprostatic incisions is a tool surgeons can use in self-audits to identify areas of potential improvement, reduce errors, and improve surgical skills.

Benign Prostate Glandular Tissue at Radical Prostatectomy Surgical Margins

To determine whether the presence of benign glandular tissue at the radical prostatectomy surgical margin is associated with technique (open radical prostatectomy [ORP] or robotic-assisted laparoscopic radical prostatectomy [RALRP]) and if benign glandular tissue increases the risk of biochemical recurrence. Surgical specimens from men with clinical T1-T2 disease who underwent radical prostatectomy (RP) between 2004 and 2010 were re-reviewed by a single uropathologist, examining all sections from the prostate apex and base for the presence of benign glandular tissue and tumor at the margin. Regression analysis was used to examine associations of benign glandular tissue with surgical approach and biochemical recurrence. Of 934 cases reviewed, 431 were managed by ORP and 503 by RALRP with a median follow-up of 49 and 28 months, respectively. Overall, benign glandular tissue was found in 274 cases (29%): 98 (36%) at the apex, 138 (50%) at the base, and 38 (14%) at both. Compared with those who underwent ORP, patients who underwent RALRP had 3-fold greater odds of benign glandular tissue at the margin (P<.01), including significantly greater number of cases with benign glandular tissue at the base (P<.01). However, recurrence-free survival rates were similar between patients with and without benign glands at the surgical margin (BGM) regardless of surgical approach and across all clinical risk groups (log-rank P= .20). Patients undergoing RALRP were more likely to have benign glandular tissue at the surgical margin. However, the presence of benign glandular tissue was not an independent risk factor for biochemical recurrence.

Digital Image Processing Technique for Breast Cancer Detection

Breast cancer is the most common cause of death in women and the second leading cause of cancer deaths worldwide. Primary prevention in the early stages of the disease becomes complex as the causes remain almost unknown. However, some typical signatures of this disease, such as masses and microcalcifications appearing on mammograms, can be used to improve early diagnostic techniques, which is critical for women’s quality of life. X-ray mammography is the main test used for screening and early diagnosis, and its analysis and processing are the keys to improving breast cancer prognosis. As masses and benign glandular tissue typically appear with low contrast and often very blurred, several computer-aided diagnosis schemes have been developed to support radiologists and internists in their diagnosis. In this article, an approach is proposed to effectively analyze digital mammograms based on texture segmentation for the detection of early stage tumors. The proposed algorithm was tested over several images taken from the digital database for screening mammography for cancer research and diagnosis, and it was found to be absolutely suitable to distinguish masses and microcalcifications from the background tissue using morphological operators and then extract them through machine learning techniques and a clustering algorithm for intensity-based segmentation.

Underestimation of Gleason score at prostate biopsy reflects sampling error in lower volume tumours

• To determine the influence of tumour and prostate gland volumes on the underestimation of prostate cancer Gleason score in diagnostic core biopsies. • Patients undergoing radical prostatectomy with matched diagnostic biopsies were identified from a prospectively recorded database. • Tumour volumes were measured in serial whole-mount sections with image analysis software as part of routine histological assessment. • Differences in various metrics of tumour and prostate volume between upgraded tumours and tumours concordant for the lower or higher grade were analysed. • In all, 684 consecutive patients with Gleason score 6 or 7 prostate cancer on diagnostic biopsy were identified. • Of 298 patients diagnosed with Gleason 6 tumour on biopsy, 201 (67.4%) were upgraded to Gleason 7 or higher on final pathology. Similarly, of 262 patients diagnosed with Gleason 3 + 4 = 7 prostate cancer on initial biopsy, 60 (22.9%) were upgraded to Gleason score 4 + 3 = 7 or higher. • Tumours upgraded from Gleason 6 to 7 had a significantly lower index tumour volume (1.73 vs 2 mL, P= 0.029), higher calculated prostate volume (41.6 vs 39 mL, P= 0.017) and lower relative percentage of tumour to benign glandular tissue (4.3% vs 5.9%, P= 0.001) than tumours concordant for the higher grade. • Similarly, tumours that were Gleason score 3 + 4 on biopsy and upgraded on final pathology to 4 + 3 were significantly smaller as measured by both total tumour volume (2.3 vs 3.3 mL, P= 0.005) and index tumour volume (2.2 vs 3, P= 0.027) and occupied a smaller percentage of the gland volume (6.3% vs 8.9%, P= 0.017) compared with tumours concordant for the higher grade. • On multivariate analysis, lower prostate weight (hazard ratio 0.97, 95% confidence interval 0.96-0.99, P < 0.001) and larger total tumour volume (hazard ratio 1.87, 95% confidence interval 1.4-2.6, P < 0.001) independently predicted an upgrade in Gleason score from 6 to 7. In tumours upgraded from biopsy Gleason 3 + 4, only higher index tumour volume (hazard ratio 3.1, 95% confidence interval 1.01-9.3, P= 0.048) was a significant predictor of upgrading on multivariate analysis. • Under-graded tumours are significantly smaller than tumours concordant for the higher grade, indicating that incomplete tumour sampling plays a significant role in Gleason score assignment error. • Surrogate measures of tumour volume may predict those at greatest risk of Gleason score upgrade.

16. Cytology of nephrogenic adenoma

<h3>Background</h3> Nephrogenic adenomas are benign lesions of the urothelial tract that are thought to arise from implantation of renal tubular epithelium in areas of chronic inflammation within the urothelium. Cytology of nephrogenic adenomas can be challenging as the cells seen can appear atypical, with papillary-like and glandular tissue fragments. In addition, variable background inflammation and degenerate cells can make the diagnosis difficult. <h3>Clinical</h3> We present the case of a 64-year-old man with biopsy proven high grade urothelial papillary carcinoma with superficial lamina propria invasion in 2009. He was treated with intravesical Bacillus Calmette-Guerin (BCG) therapy. Subsequent urine cytology reports ranged from ‘atypical cells', ‘cells suspicious for carcinoma' and ‘malignant urothelial carcinoma'. Multiple concurrent urothelial biopsies showed chronic inflammation and nephro-genic adenomas. Only one of these biopsies showed dysplasia. <h3>Cytology</h3> On review, multiple bladder, left pelvic and right pelvic washings showed similar features consistent with nephrogenic adenoma including glandular tissue fragments in a mild to moderate background of inflammation. The cells had enlarged hyper-chromatic nuclei, uniform nuclear membranes, and evenly distributed chromatin with clear cytoplasm, and occasional cells with cytoplasmic vacuoles. <h3>Discussion</h3> Distinguishing nephrogenic adenoma from malignant diagnoses is important in terms of ongoing surveillance and treatment. Recognition of nephrogenic adenomas in urine cytology can be difficult and as in this case can be mistaken for urothelial carcinoma. Other differentials include adenocarcinoma, either renal, urothelial or prostatic in origin, and reactive changes due to chemotherapy, instrumentation or surgery. Cytological features of nephrogenic adenoma may display atypia, however the cells usually do not reach the cytological criteria for malignancy. The presence of benign glandular tissue fragments in bilateral pelvic washings supports current theories that nephrogenic adenomas arise from implantation of renal tubular cells.

1555 THE RISK OF IATROGENIC POSITIVE MARGIN IN RADICAL PROSTATECTOMY: AN EXPENDED CRITERION TO EVALUATE THE QUALITY OF SURGICAL RESECTION

You have accessJournal of UrologyProstate Cancer: Localized VI1 Apr 20101555 THE RISK OF IATROGENIC POSITIVE MARGIN IN RADICAL PROSTATECTOMY: AN EXPENDED CRITERION TO EVALUATE THE QUALITY OF SURGICAL RESECTION Christian Barré, Geneviève Aillet, and Matthieu Thoulouzan Christian BarréChristian Barré Nantes, France More articles by this author , Geneviève AilletGeneviève Aillet Nantes, France More articles by this author , and Matthieu ThoulouzanMatthieu Thoulouzan Toulouse, France More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2010.02.1320AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Conventionally, the rate of positive surgical margins (PSM) for pT2 tumors, i.e. iatrogenic positive margins (IPM), is taken as the technical error rate. However, this is not a good indicator of technical error as it concerns dissection errors involving only malignant and not benign tissue. The technical error rate should also include the risk of IPM i.e. all incisions of benign tissue within the histological limits of the prostate defined by McNeal because the incised tissue might just as well have been malignant as benign. Even if the benign proved to be benign, this did not eliminate the risk that was run. The safety of a technique does not depend only on the known consequences of an error such as a PSM (″adverse events″) but also on the number of times errors with potentially deleterious consequences are made (″near-misses″). The aim of this prospective study was to establish expanded criteria for evaluating the quality of surgical resection in patients undergoing radical retropubic prostatectomy (RRP). METHODS Prospective study (Jan 2005-Dec 2007), 507 consecutive patients with localised prostate cancer underwent RRP. We determined the rate of IPM and PSM. Pathological study: whole-mount 3-mm serial sections using the Stanford technique. Where capsule was absent (apex and bladder neck) no malignant or benign gland must be in contact with the inked margin. In the capsular zone, we defined 1st degree capsule incision (1st DCI): loss of the outer connective tissue layer and 2nd degree capsule incision (2nd DCI): loss of both capsule layers with malignant or benign gland in contact with ink. RESULTS Patient characteristics were mean age 61.3 years; disease stage: pT2 73%, pT3 25.8%; bilateral nerve-sparing n=273, 88.1%, unilateral n=37, 11.9%. The risk of IPM was 5%: incision of benign glandular tissue was 2.8% (apex: 43%; bladder neck: 57%), 1st DCI was 2.2% and 2nd DCI was 0%. The overall PSM rate was 6.3%: 2.2 % (8/370) for pT2, 14.5 % (19/131) for pT3, and 83.3% for pT4. It was 4.8% (15/310) in patients undergoing nerve-sparing surgery. PSM with pT2 tumours occurred at apex (1.7%), postero-lateral 0%, bladder neck (0.5%). PSMs with pT3a/b tumours occurred at: apex (6.1%), postero-lateral (3.8%) and bladder neck (6.9%). PSM size distribution for pT2: PSM≤1 mm: n=4; 1<PSM≤4 mm: n=2; PSM >4 mm: n=2, and for pT3: PSM≤1 mm: n=6; 1<PSM≤4 mm: n=5; PSM>4 mm: n=8. Biochemical recurrence rate (PSA >0.10 ng/ml) at 1 year was 2.6%. CONCLUSIONS The safety of an RP procedure is given not only by the PSM rate for pT2 tumours but also by the percentage of times there is a risk of a PSM. © 2010 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 183Issue 4SApril 2010Page: e600 Advertisement Copyright & Permissions© 2010 by American Urological Association Education and Research, Inc.MetricsAuthor Information Christian Barré Nantes, France More articles by this author Geneviève Aillet Nantes, France More articles by this author Matthieu Thoulouzan Toulouse, France More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

A monoclonal antibody cytolytic to androgen independent DU145 and PC3 human prostatic carcinoma cells

Background While a range of therapeutic products is available for androgen-dependent prostatic cancer, no specific intervention modality exists for androgen-independent prostatic cancer. The objective of this research was to explore whether epitopes exist on androgen-independent prostatic DU145 cancer cells, which could be susceptible to cytotoxic action of specific antibodies. Methods Hybrid cell clones were developed by immunization of mice with DU145 cells and tested for immunoreactivity by solid phase EIA and cytotoxicity in vitro on DU145 in the presence of the complement, employing colorimetric quantitation by MTS (3- (4-, 5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-(4-sulfophenyl)-2H-tetrazolium). Binding and cytotoxicity studies were also carried out by flow-cytometry. Results Of 15 stabilized clones immunoreactive with DU145 cells, one monoclonal antibody (mAb 730) manifested cytotoxicity on DU145 cells. Approximately 80% of cells in the DU145 cell line were susceptible to lysis with this antibody at saturating levels. This figure corresponded quantitatively to the number of cells binding with this antibody as determined by Flow-cytometry. Staining with ethidium monoazide bromide (EMA) showed that the cell binding the antibody was also the one killed by the antibody in the presence of the complement. MAb 730 was also cytotoxic to PC3, another androgen-independent human prostatic cancer cell line. This antibody is devoid of classical autoantibody reactivities and does not react with normal human liver, thyroid, kidney, pancreas, and adrenal tissues, as determined by immunofluorescence. Also, it shows negative immuno-reactivity to benign glandular tissue but is observed to positively react with neoplastic prostate tissue. Conclusions Epitopes exist on androgen-independent prostatic cancer cells that are susceptible to cytolysis by monoclonal antibodies and these could be investigated for potential immunotherapy. Prostate 46:207–213, 2001. © 2001 Wiley-Liss, Inc.

A monoclonal antibody cytolytic to androgen independent DU145 and PC3 human prostatic carcinoma cells.

While a range of therapeutic products is available for androgen-dependent prostatic cancer, no specific intervention modality exists for androgen-independent prostatic cancer. The objective of this research was to explore whether epitopes exist on androgen-independent prostatic DU145 cancer cells, which could be susceptible to cytotoxic action of specific antibodies. Hybrid cell clones were developed by immunization of mice with DU145 cells and tested for immunoreactivity by solid phase EIA and cytotoxicity in vitro on DU145 in the presence of the complement, employing colorimetric quantitation by MTS (3- (4-, 5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-(4-sulfophenyl)-2H-tetrazolium). Binding and cytotoxicity studies were also carried out by flow-cytometry. Of 15 stabilized clones immunoreactive with DU145 cells, one monoclonal antibody (mAb 730) manifested cytotoxicity on DU145 cells. Approximately 80% of cells in the DU145 cell line were susceptible to lysis with this antibody at saturating levels. This figure corresponded quantitatively to the number of cells binding with this antibody as determined by Flow-cytometry. Staining with ethidium monoazide bromide (EMA) showed that the cell binding the antibody was also the one killed by the antibody in the presence of the complement. MAb 730 was also cytotoxic to PC3, another androgen-independent human prostatic cancer cell line. This antibody is devoid of classical autoantibody reactivities and does not react with normal human liver, thyroid, kidney, pancreas, and adrenal tissues, as determined by immunofluorescence. Also, it shows negative immuno-reactivity to benign glandular tissue but is observed to positively react with neoplastic prostate tissue. Epitopes exist on androgen-independent prostatic cancer cells that are susceptible to cytolysis by monoclonal antibodies and these could be investigated for potential immunotherapy.

RADICAL PROSTATECTOMY FOR PROSTATE CANCER: THE PERINEAL APPROACH INCREASES THE RISK OF SURGICALLY INDUCED POSITIVE MARGINS AND CAPSULAR INCISIONS

Purpose We compare the incidence of positive surgical margins in patients who underwent perineal or retropubic radical prostatectomy for clinically localized (stage T1, T2) prostate cancer. Materials and Methods In this retrospective, nonrandomized study we reexamined the specimens of 94 consecutive patients who underwent radical perineal (48) or retropubic (46) prostatectomy for clinically localized prostate cancer (stage T1, T2) and with pathological stage pT2 (intracapsular), pT3A (established extracapsular extension without positive margins) or pT3B (extracapsular extension with positive margins) without lymph node involvement (N0). We assessed the presence or absence of extracapsular cancer with or without positive margins, incisions of the prostatic capsule exposing cancer (surgically induced positive margins) or benign glandular tissue. Patients were followed for 3 to 66 months (mean 25) using an ultrasensitive prostate specific antigen assay with a lower detection limit of less than 0.05 ng./ml. Results The overall incidence of positive margins in cancer tissue was 56% in the perineal and 61% in the retropubic group, and biochemical failure-free survival was 67% each. However, surgically induced positive margins in patients with organ confined disease were more frequent in the perineal than retropubic group (43 versus 29%, p <0.05) and associated with a 37% risk of biochemical failure (prostate specific antigen greater than 0.1 ng./ml.) at mean followup. In addition, capsular incisions exposing benign tissue were more frequent in the perineal than retropubic group (90 versus 37%, p <0.05) irrespective of pathological stage. Conclusions Although overall positive margins and biochemical failure rates are similar or identical for the perineal and retropubic approaches for organ confined prostate cancer, the perineal approach is associated with a significantly higher risk of capsular incisions and surgically induced positive margins and, thus, a higher risk of biochemical failure.

Short-term outcomes after cryosurgical ablation of the prostate in men with recurrent prostate carcinoma following radiation therapy

Cryosurgical ablation of the prostate represents a possibly efficacious method of treating prostate carcinoma in men failing radiation therapy. In addition to eradicating the disease, cryosurgery has the potential to avoid some of the morbidity associated with other treatment modalities. Therefore, a prospective Phase II trial was conducted to determine the safety and efficacy of cryosurgery following radiation therapy in men with local recurrence. Cryosurgical ablation of the prostate was performed in men with prostate cancer previously treated by radiation therapy. All patients had biopsy-proven recurrent disease and no evidence of metastases. Initial follow-up occurred at approximately 3 months and included repeat biopsy and serum prostate-specific antigen (PSA) determinations. Biochemical disease-free survival defined as a PSA value less than 0.3 ng/mL was assessed using the Kaplan-Meier method. Thus far, 23 patients have been treated with cryosurgery with follow-up ranging between 12 and 23 months. Approximately 3 months after treatment, sextant biopsies revealed no cancer in 19 of 22 (86%) of the specimens; however, 10 of 22 (45%) showed small amounts of benign glandular tissue. The PSA at 3 months postoperatively declined in 18 of 22 (82%) patients but reached female levels in only 8 men (36%). Nineteen of 22 (86%) patients followed up a minimum of 1 year after cryotherapy have a PSA level equal to or greater than 0.3 ng/mL. Complications occurred in 100% of the patients with 12 of 22 (55%) requiring at least one transurethral resection of sloughed, necrotic tissue. Our preliminary results suggest that the current cryosurgical technique used in men failing radiation therapy has a low probability of biochemical cure and a high complication rate. Until more data are available, cryosurgery for men with locally recurrent disease after radiation therapy should be considered strictly experimental.

Comparison of microscopic vascularity in benign and malignant prostate tissue

A variety of malignant neoplasms have been shown to induce capillary neovascularization, and in some cases the degree of vascularization appears to correlate with aggressive behavior and risk of metastasis. We hypothesized that carcinoma of the prostate also induces the formation of new capillaries, and we developed a method to quantify the relative density of microscopic vessels in carcinoma of the prostate compared with benign prostatic glandular tissue. The number of microvessel profiles in tissue sections was quantified by marking the vascular endothelial cells with antibodies to factor VIII-related antigen using standard immunohistochemistry techniques and comparing fields of adenocarcinoma with benign glandular tissue in 15 radical prostatectomy specimens. The analysis was facilitated by using the Optimas computerized image analysis system (Bioscan, Seattle, WA) with software written for this investigation. Fourteen of the 15 cases demonstrated significantly higher vascular density in the areas of carcinoma than in the benign tissues. Overall, the ratio of vessels per unit area in sections of carcinoma versus benign tissue was approximately double (ratio = 2.02; P < .001). In benign tissues the capillaries are restricted for the most part to the periglandular stroma immediately adjacent to the epithelium, whereas the distribution in carcinoma appears to be more random. The data demonstrate the increased density of capillaries in prostatic carcinoma when compared with benign prostate tissue.