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Patrick C Walsh

Publications and source records attributed to Patrick C Walsh.

At least 91 records · Page 5Linked to original sources
PubMed2004

Impact of surgical delay on long-term cancer control for clinically localized prostate cancer.

PURPOSE: Radical retropubic prostatectomy (RRP) as definitive management for clinically localized prostate cancer is commonly performed within months of diagnosis. Despite patient anxiety there is little evidence to suggest that a delay of several months from diagnosis to RRP is associated with a worse cancer control rate. However, a recent study cast doubt on the safety of such a delay with respect to cancer control. Therefore, in a contemporary series we determined long-term cancer control in men who underwent RRP for clinically localized prostate cancer with some treated early and others treated after a longer delay. MATERIALS AND METHODS: We analyzed data on 926 men who underwent RRP between January 1989 and December 1994. Age, preoperative serum prostate specific antigen (PSA), biopsy Gleason score, clinical and pathological stage, and biochemical recurrence were compared between 162 men who underwent RRP 60 days or less from biopsy and 764 who underwent RRP after a greater delay. Disease-free (PSA less than 0.2 ng/ml) survival rates were compared using Kaplan-Meier analysis. Pathological staging was compared using logistic regression. RESULTS: The different groups were well matched for age, serum PSA, pathological stage and followup. However, significantly more men who underwent RRP between 121 and 150 days, and 151 days or greater had T1c disease (48% and 57% vs 35%, p<0.04 and <0.0001, respectively). In addition, significantly more men operated on at 151 days or greater had biopsy Gleason scores 2 to 6 (86% vs 65%, p<0.0001) and significantly fewer had Gleason score 7 disease (13% vs 30%, p<0.002). Men who underwent RRP after 60 or less days had 5 and 10-year biochemical disease-free survival rates comparable to those in men who underwent RRP after 61 to 90, 91 to 120 and 121 to 150 days after diagnosis (82% and 78%, 86% and 78%, 86% and 75%, and 86% and 82%, respectively). Those operated on at 151 days or greater had significantly greater 5 and 10-year biochemical disease-free survival rates (89% and 87%, p<0.04). However, when patients were stratified into different subgroups based on clinical stage, serum PSA and biopsy Gleason score a delay of 150 days or greater no longer impacted differently on long-term cancer control rates. CONCLUSIONS: Delays of up to several months from prostate cancer diagnosis to RRP do not appear to impact long-term biochemical cancer control rates. Therefore, patients can be reassured that there is no immediate urgency to perform RRP after prostate cancer diagnosis, especially in those with T1c disease and biopsy Gleason scores less than 7.

Adenocarcinoma↗
PubMed2004

Anatomical extent of lymph node dissection: impact on men with clinically localized prostate cancer.

PURPOSE: This study evaluates the influence of the anatomical extent of pelvic lymph node dissection performed at radical prostatectomy on lymph node yield, staging accuracy and time to prostate specific antigen progression. MATERIALS AND METHODS: Between February 1992 and April 2003, 2 surgeons at 1 hospital performed 2,135 and 1,865 radical prostatectomies with pelvic lymph node dissection, respectively. One surgeon routinely performed an extended lymph node dissection while the second surgeon performed a limited pelvic lymphadenectomy. The number of lymph nodes extracted and the number of patients with positive lymph nodes detected were analyzed and compared. Kaplan-Meier analysis was used to compare the biochemical recurrence-free survival between the 2 groups of patients with occult nodal disease. RESULTS: Extended lymph node dissection removed more lymph nodes (mean 11.6 vs 8.9, p<0.0001) and detected more lymph node positive disease (3.2% vs 1.1%, p<0.0001) than the more anatomically limited technique. This finding held true for patients across all pathology groups. Among men with lymph node positive disease involving less than 15% of extracted nodes, the 5-year prostate specific antigen progression-free rate for extended lymph node dissection was 43% versus 10% for the more limited lymph node dissection (p = 0.01). CONCLUSIONS: Compared to limited lymph node dissection, extended pelvic lymphadenectomy appears to identify men with positive lymph nodes more frequently. A significant benefit in biochemical recurrence-free survival may exist for certain subgroups undergoing the extended dissection. However, because the results may be influenced by stage migration, longer followup is necessary to determine whether the apparent therapeutic effect persists.

Adult↗
PubMed2004

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Journal Article↗
PubMed2003

Prostate-specific antigen doubling time in the identification of patients at risk for progression after treatment and biochemical recurrence for prostate cancer.

After primary treatment for clinically localized prostate cancer, biochemical recurrence is usually the first evidence of either local recurrence or metastatic progression. This poses a diagnostic dilemma for both the patient and the physician regarding future therapy. Prostate-specific antigen doubling time (PSADT) is a useful tool in this clinical setting. There have been multiple reports of the utility of PSADT in men with isolated biochemical recurrence after either radical prostatectomy or external-beam radiation therapy. Early observations of PSADT in men with recurrence are reviewed and the current literature is summarized to allow physicians to make an accurate assessment of a patient's risk of progression after isolated biochemical recurrence.

Adenocarcinoma↗
PubMed2003

Quantitative alterations in nuclear structure predict prostate carcinoma distant metastasis and death in men with biochemical recurrence after radical prostatectomy.

BACKGROUND: Microscopic histologic grade has been the best predictor of prostate carcinoma (PCa) progression in men after surgical therapy. The ability to predict accurately, at the time of surgery, which patients are likely to develop metastatic PCa would enable optimization of disease management with adjuvant therapy. The authors assessed the ability of pathologic, nuclear morphometric, and chromatin parameters to predict metastatic PCa progression and/or death in 227 men with biochemical recurrence and long-term follow-up after undergoing radical prostatectomy. METHODS: Multivariate logistic regression (LR) was used to calculate quantitative nuclear grade (QNG) solutions using the variances of 60 nuclear morphometric descriptors (NMDs) of nuclear size, shape, DNA content, and chromatin organization that predicted distant metastasis and/or PCa-specific death. An LR model also was generated to predict this outcome using a combination of pathologic variables and the best QNG solution. Cox proportional hazards models were generated, and Kaplan-Meier plots were used to display three risk groups based on pathology, QNG, and a combination of these variables. RESULTS: A multivariate LR model using pathology retained lymph node (LN) status, seminal vesicle status, and prostatectomy Gleason score, yielding an area under the curve-receiver operator characteristic (AUC-ROC) of 75% with an accuracy of 59% at 90% sensitivity. The best QNG solution used the variance of 25 NMDs, yielding an AUC-ROC of 84% and an accuracy of 70% at 90% sensitivity. The combined pathology-QNG model retained LN status, prostatectomy Gleason score, and QNG, yielding an AUC-ROC of 86% with an accuracy of 76% at 90% sensitivity. The Cox proportional hazards models produced the following significant univariate and multivariate hazard ratios: QNG, 3.5 and 2.9, respectively; LN, 2.7 and 1.8, respectively; and prostatectomy Gleason score, 2.8 and 2.1, respectively. CONCLUSIONS: Alterations in the structure of tumor nuclei measured by computer-assisted image analysis were strong predictors of PCa progression and death in men with long-term follow-up who had biochemical recurrence after undergoing radical prostatectomy. QNG solutions can serve as a new supplemental biomarker for accurate prediction of PCa progression at the time of surgery.

Adenocarcinoma↗
PubMed2003

Genome-wide scan for prostate cancer susceptibility genes in the Johns Hopkins hereditary prostate cancer families.

BACKGROUND: Although the subject of intensive study, the genetic influences responsible for familial clustering of prostate cancer remain largely unidentified. Genome-wide scans for linkage in prostate cancer families can be used to systematically search for genes capable of affecting risk for the disease. METHODS: All available family members from 188 families, each having at least three first-degree relatives affected with prostate cancer, were genotyped at 406 markers distributed across the genome at average intervals of less than 10 cM. Genotype data was analyzed using primarily a non-parametric, multipoint approach, although parametric analyses were performed as well. RESULTS: The strongest evidence for linkage was observed at D4S1615, at 4q21 (LOD of 2.8, P = 0.0002). Two other regions had LOD scores over 2.0: at 9q34 (marker D9S1826, LOD = 2.17, P = 0.0008) and at 2q23 (marker D2S151, LOD = 2.03, P = 0.001). An additional 12 regions had LOD scores over 1.0, including markers at 1q24-25 and 7q22 having scores >1.6. Stratifying the linkage results by age of diagnosis indicated that the linkages to chromosomes 2 and 4 were strongest in families with early and late ages of diagnosis, respectively. CONCLUSIONS: Our data implicate several new loci as harboring prostate cancer susceptibility genes, and provide confirmatory evidence of linkage at several loci identified previously in other genome-wide scans, including the three regions (4q21, 9q34, and 2q23) with strongest evidence for prostate cancer linkage. These data also emphasize the need to combine linkage data from large numbers of prostate cancer families in efforts to effectively address the extensive heterogeneity that characterizes genetic aspects of this disease.

Aged↗
PubMed2003

Quantitative GSTP1 methylation and the detection of prostate adenocarcinoma in sextant biopsies.

Hypermethylation of the 5' promoter region of the glutathione S-transferase pi gene (GSTP1) occurs at a very high frequency in prostate adenocarcinoma. We compared the results of blinded histologic review of sextant biopsy samples from 72 excised prostates with those obtained using a quantitative methylation-specific polymerase chain reaction assay (QMSP) for GSTP1. Formal surgical pathologic review of the resected prostates was used to determine the number of patients with (n = 61) and without (n = 11) prostate cancer. Histology alone detected prostate carcinoma with 64% sensitivity (95% confidence interval [CI] = 51% to 76%) and 100% specificity (95% CI = 72% to 100%), whereas the combination of histology and GSTP1 QMSP at an assay threshold greater than 10 detected prostate carcinoma with 75% sensitivity (95% CI = 63% to 86%) and 100% specificity (95% CI = 72% to 100%), an 11% improvement (95% CI = 5% to 22%) in sensitivity over histology alone. The combination of histology and GSTP1 QMSP at an assay threshold greater than 5 detected prostate adenocarcinoma with 79% sensitivity (95% CI = 68% to 89%), a 15% improvement (95% CI = 7% to 26%) over histology alone. Thus, GSTP1 QMSP improved the sensitivity of histologic review of random needle biopsies for prostate cancer diagnosis. Further studies should determine whether detection of GSTP1 hypermethylation in a biopsy sample with normal histology indicates the need for an early repeat biopsy at the same site.

Adenocarcinoma↗
PubMed2003

Decreased gene expression of steroid 5 alpha-reductase 2 in human prostate cancer: implications for finasteride therapy of prostate carcinoma.

BACKGROUND: Steroid 5alpha-reductase 2 (SRD5A2) catalyzes the conversion of testosterone to the more potent androgen, DHT, in the prostate. The therapeutic influence of SRD5A2 inhibitor finasteride on prostate cancer is currently unknown. The direction and extent of changes in SRD5A2 expression in disease tissues is a relevant issue in this regard. METHODS: The expression differences of SRD5A2 in tissues representative of normal, benign, and malignant growth in the human prostate were examined in parallel by comparative analysis of relevant microarray gene expression data. Semiquantitative RT-PCR was used to further verify the gene expression differences of SRD5A2. RESULTS: Consistently decreased expression of SRD5A2 was observed in 25 prostate cancer samples when compared to 25 matched normal samples and nine BPH samples. Expression differences among these samples for six other genes were presented in parallel as indicators of the direction and extent of expression changes. These additional genes include SRD5A1, Hepsin (overexpressed in prostate cancer), AMACR (overexpressed in prostate cancer), Keratin 8 (epithelial marker), smooth muscle actin (stromal marker), Nell2 (overexpressed in BPH). Semiquantitative RT-PCR verified the expression differences for SRD5A2 in six normal, six BPH, and six prostate cancer samples. CONCLUSIONS: Results from this study, combined with those from previous studies, indicate an association of prostate cancer with reduced 5alpha-reductase enzymatic activity as a result of remarkably decreased expression of the SRD5A2 gene. The implications of this study for finasteride therapy of prostate cancer are discussed.

Case-Control Studies↗
PubMed2003

Polymorphisms in the CYP1A1 gene are associated with prostate cancer risk.

CYP1A1 is likely to play an important role in the etiology of CaP through its function in activating environmental procarcinogens and catalyzing the oxidative metabolites of estrogens. To test the hypothesis that genetic polymorphisms in the CYP1A1 gene may be associated with the risk for CaP, we compared the allele, genotype and haplotype frequencies of 3 SNPs (3801T>C, 2455A>G and 2453C>A) of CYP1A1 among 159 HPC probands, 245 sporadic CaP cases and 222 unaffected men. Two SNPs (3801T>C and 2455A>G) were each individually associated with CaP risk when the allele and genotype frequencies were compared between CaP patients and unaffected controls. Furthermore, a combined SNP analysis using a haplotype approach revealed an even stronger association in Caucasians. Specifically, 4 major haplotypes (T-A-C, C-A-C, C-G-C and T-A-A) accounted for 99.8% of all observed haplotypes. These 4 haplotypes correspond to the previously described nomenclature (CYP1A1*1A, CYP1A1*2A, CYP1A1*2B and CYP1A1*4). The frequencies of these 4 haplotypes were significantly different among CaP patients and controls. The haplotype T-A-C (CYP1A1*1A) was significantly associated with increased risk for CaP, and the haplotype C-A-C (CYP1A1*2A) was significantly associated with decreased risk for CaP. These findings suggest that genetic polymorphisms in CYP1A1 may modify the risk for CaP.

Biomarkers, Tumor↗
PubMed2003

Evaluation of DLC1 as a prostate cancer susceptibility gene: mutation screen and association study.

A gene or genes on chromosome 8p22-23 have been implicated in prostate carcinogenesis by the observation of frequent deletions of this region in prostate cancer cells. More recently, two genetic linkage studies in hereditary prostate cancer (HPC) families suggest that germline variation in a gene in this region may influence prostate cancer susceptibility as well. DLC1 (deleted in liver cancer), a gene in this interval, has been proposed as a candidate tumor suppressor gene because of its homology (86% similarity) with rat p122 RhoGAP, which catalyzes the conversion of active GTP-bound rho complex to the inactive GDP-bound form, and thus suppresses Ras-mediated oncogenic transformation. A missense mutation and three intronic insertions/deletions in 126 primary colorectal tumors have been previously identified. However, there are no reports of DLC1 mutation screening in prostate tumors or in germ line DNA of prostate cancer patients. In this study, we report the results of the first mutation screen and association study of DLC1 in genomic DNA samples from hereditary and sporadic prostate cancer patients. The PCR products in the 5' UTR, all 14 exons, exon-intron junctions, and 3' UTR were directly sequenced in 159 HPC probands. Eight exonic nucleotide polymorphisms (SNPs) were identified, only one of which resulted in an amino acid change. Twenty-three other SNPs were identified in intronic regions. Seven informative SNPs that spanned the complete DLC1 gene were genotyped in an additional 249 sporadic cases and 222 unaffected controls. No significant difference in the allele and genotype frequencies were observed among HPC probands, sporadic cases, and unaffected controls. These results suggest that DLC1 is unlikely to play an important role in prostate cancer susceptibility.

GTPase-Activating Proteins↗
PubMed2003

Evaluation of SRD5A2 sequence variants in susceptibility to hereditary and sporadic prostate cancer.

BACKGROUND: The 5 alpha-reductase type II (SRD5A2) catalyzes the conversion of testosterone into the more potent androgen, dihydrotestosterone (DHT), and is thus believed to be the key enzyme for the control of intracellular DHT level in the prostate. Several single nucleotide polymorphisms (SNPs) in the SRD5A2 gene have been found to alter enzymatic activities and were associated with prostate cancer risk or clinical features in several case-control studies. However, the role of SRD5A2 sequence variants in the susceptibility to hereditary prostate cancer (HPC) has not been evaluated to date. METHODS: Three SNPs in the SRD5A2 gene (A49T, V89L, and C682G) and two microsatellite markers near SRD5A2 were genotyped in 159 HPC families to assess their linkage to prostate cancer. In addition, the three SNPs were also genotyped in 245 sporadic cases and 222 unaffected controls to assess their association with hereditary and sporadic prostate cancer. RESULTS: Weak evidence for linkage in the SRD5A2 chromosomal region was observed in the 159 HPC families (HLOD = 0.87, P = 0.04). Stronger evidence for linkage was observed in Caucasian families (HLOD = 1.10, P = 0.02). When stratified by the SNP A49T, no significant evidence for linkage was observed in families with or without the "T" allele. Similarly, family-based association tests failed to observe significant over-transmission of any risk alleles of SNPs A49T, V89L, and C682G to affected offspring. Finally, no significant differences in the distributions of SNPs A49T, V89L, and C682G were found among the HPC probands, sporadic cases, and controls. CONCLUSIONS: Polymorphisms of SRD5A2 are unlikely to significantly increase susceptibility to hereditary or sporadic prostate cancer in the study populations.

Aged↗
PubMed2003

Family history of prostate cancer and obesity in relation to high-grade disease and extraprostatic extension in young men with prostate cancer.

BACKGROUND: Little is known about predictors of prostate cancer severity in young men. Therefore, we examined whether family history and obesity influence risk of high-grade disease and extraprostatic extension in men < 55-years old. METHODS: Four hundred ninety-eight men aged < 55 years who had had a radical prostatectomy (1992-1999) by one surgeon were mailed a survey in 2000 to assess family history of PCa and anthropometrics. Body mass index (BMI = kg/m(2)) was calculated as an indicator of obesity. Logistic regression was used to compute odds ratios (OR) for high-grade disease (Gleason score > or = 7) and extraprostatic extension. RESULTS: Of the 363 respondents, 35.8% had at least one first-degree relative with PCa. Men with a family history were younger at surgery than those without a family history (48.8 vs. 50.1 years, P < 0.001). After controlling for age, cigarette smoking, and race/ethnicity, men with an affected father had a lower risk of high-grade disease compared to those without an affected father (OR = 0.42, 95% CI 0.23-0.76). Risk of high-grade disease increased with increasing BMI, especially in men < 50-years old (P-trend = 0.02). Family history and BMI were not clearly associated with extraprostatic extension. CONCLUSIONS: After taking into account a younger age at presentation among men with a family history, young men with a family history of PCa were less likely to have high-grade disease. Obesity may be associated with a poorer histology in young men with PCa, especially in men younger than 50 years of age.

Body Mass Index↗
PubMed2003

Balloon cuffing and management of the entrapped Foley catheter.

We have experienced the inability to remove silicone Foley catheters even after complete deflation of the balloon. This potential complication can result from cuffing of the catheter balloon. We present a description of this phenomenon and approaches for successful management of a Foley catheter that has become entrapped due to balloon cuffing.

Catheterization↗
PubMed2003

Familial aggregation of bothersome benign prostatic hyperplasia symptoms.

OBJECTIVES: To evaluate familial aggregation and the mode of inheritance of bothersome benign prostatic hyperplasia (BPH). METHODS: During an extension of the North American Finasteride Trial, 301 of 895 patients and 158 spousal controls completed a family history questionnaire. Segregation analysis was performed to examine the mode of inheritance in first-degree relatives of the 301 probands. RESULTS: The lifetime cumulative probability of bothersome BPH was similar in relatives of those with BPH (0.35; 95% confidence interval [CI] 0.28 to 0.44) and spousal controls (0.36; 95% CI 0.22 to 0.56), but the age of onset was significantly earlier in relatives of cases than controls (P = 0.001). Fathers of those with BPH had a significantly elevated risk of bothersome BPH (unadjusted odds ratio [OR] 2.1; 95% CI 1.2 to 3.8) and brothers had a significantly elevated risk of both bothersome BPH (OR 3.5; 95% CI 1.7 to 7.3) and transurethral resection of the prostate (OR 3.6; 95% CI 1.4 to 8.8). After adjusting for family size, the risk of bothersome BPH increased approximately twofold with each additional affected first-degree relative (0 relatives, OR 1.0; 1 relative, OR 1.7; 2 relatives, OR 4.7). Segregation analysis suggested a rare autosomal codominant allele (frequency 0.0004). CONCLUSIONS: These findings confirm previous findings that family history and early age of onset are associated with an increased risk of BPH and that the most likely mode of inheritance is autosomal dominant or codominant. Bothersome BPH appears to have a weaker genetic component than more restrictive definitions of hereditary BPH. Thus, linkage studies are more likely to be successful if they focus on stricter definitions of hereditary BPH (eg, early onset, large volume, strong family history) rather than symptomatic or clinical BPH.

Adult↗
PubMed2003

Long-term 6-year experience with finasteride in patients with benign prostatic hyperplasia.

OBJECTIVES: To summarize the 6-year clinical trial data with finasteride. Benign prostatic hyperplasia is a chronic and progressive disease and therefore assessment of long-term safety and efficacy is important. METHODS: The North American and International Phase III Finasteride trials enrolled symptomatic men with enlarged prostate glands. The initial 1-year placebo-controlled study was followed by a 5-year open-label extension. In total, 6-year finasteride data were available in 487 patients originally randomized to finasteride, and 5-year data were available on 238 patients originally randomized to placebo. RESULTS: After 6 years of treatment with finasteride 5 mg, the mean quasi-American Urological Association Symptom Score improved by 4.0 points, the median prostate volume decreased by 24%, and the mean maximal urinary flow rate increased by 2.9 mL/s (P <0.001 for all parameters). Long-term finasteride treatment was well tolerated, with a low incidence of drug-related sexual adverse events occurring during the first year and even fewer occurrences during the 5-year open extension. CONCLUSIONS: Treatment with finasteride leads to durable improvement in urinary tract symptoms, flow rate, and prostate volume, with no increase in the prevalence of drug-related adverse events over time.

5-alpha Reductase Inhibitors↗
PubMed2003

Long-term cancer control of radical prostatectomy in men younger than 50 years of age: update 2003.

OBJECTIVES: To compare the cancer control in men younger than 50 years with that in older men treated with radical retropubic prostatectomy (RRP) for localized prostate cancer in a contemporary series. In the 1970s and 1980s, men younger than 50 years old represented approximately 1% of newly diagnosed prostate cancer cases. However, with the widespread use of serum prostate-specific antigen (PSA) testing and increased public awareness of prostate cancer, this figure has risen (3.7% to 4%). Previous studies, mostly carried out before the PSA era, reported conflicting data with respect to cancer control for these younger men treated with RRP. METHODS: We analyzed the data from 2897 men who underwent RRP between April 1982 and September 2001. Preoperative PSA level, clinical and pathologic stage, and biochemical recurrence were compared between 341 men younger than 50 years old and 2556 men 50 years old or older. Disease-free (PSA less than 0.2 ng/mL) survival rates were compared using Kaplan-Meier analysis. Pathologic staging was compared using logistic regression analysis. RESULTS: Men younger than 50 years old had pathologic variables and 5, 10, and 15-year biochemical disease-free survival rates comparable to men aged 50 to 59 years (88%, 81%, and 69% versus 87%, 78%, and 71%, respectively). However, younger men had a lower incidence of extraprostatic extension (25% versus 31%; P <0.02), seminal vesicle involvement (2% versus 6%; P <0.03), and positive surgical margins (3% versus 9%; P <0.03), a greater organ-confined disease rate (65% versus 49%; P <0.0001), and a trend toward greater 5, 10, and 15-year biochemical disease-free survival rates, which did not reach statistical significance, compared with men aged 60 to 69 years (84%, 74%, and 67%, respectively; P <0.09). Furthermore, younger men not only had a lower rate of extraprostatic extension (25% versus 36%; P <0.001), seminal vesicle involvement (2% versus 10%; P <0.001), and positive surgical margins (3% versus 9%; P <0.001) and a greater organ-confined disease rate (65% versus 36%; P <0.0001), they also demonstrated significantly (P <0.003) greater 5, 10, and 15-year biochemical disease-free survival rates compared with men aged 70 years or older (72%, 58%, and 58%, respectively). CONCLUSIONS: Men diagnosed with prostate cancer who are younger than 50 years of age and are candidates for RRP tend to have a greater probability of organ-confined disease than older men. Younger men also demonstrate greater long-term cancer control rates than older men.

Adenocarcinoma↗
PubMed2003

Probability of biochemical recurrence by analysis of pathologic stage, Gleason score, and margin status for localized prostate cancer.

OBJECTIVES: The Partin tables provide pretreatment information regarding the probability of various pathologic stages (eg, organ confined, extraprostatic extension, and seminal vesicle or lymph node involvement). Although the pathologic stage serves as an excellent surrogate for outcome after radical prostatectomy (RRP), many patients and physicians want to know how the predictions made from the Partin tables can be translated into long-term biochemical recurrence-free survival. In this work, we go beyond the pathologic outcomes predicted by the Partin nomograms to provide long-term biochemical recurrence-free estimates on the basis of the pathologic data obtained at RRP to help counsel patients after surgery for prostate cancer. METHODS: The study group comprised 1955 men treated by one surgeon with RRP and pelvic lymph node dissection for clinically localized disease (1989 to 2001). The patients were followed up for at least 1 year postoperatively, and the disease-free survival rates were determined using Kaplan-Meier analysis. RESULTS: The pathologic stages were as follows: organ confined in 57%, extraprostatic extension in 35%, seminal vesicle involvement in 4%, and lymph node involvement in 4%. The prostatectomy Gleason score distribution was as follows: 2 to 4 in 1%, 5 to 6 in 63%, 7 in 30%, and 8 to 10 in 6%. Overall, a positive surgical margin was present in 9.8%. On the basis of the prostatectomy Gleason score, pathologic stage, and surgical margin status, the probability of long-term biochemical recurrence-free survival was divided into four groups: excellent, good, moderate, and low. CONCLUSIONS: These simple to use and explain risk groups can be used to predict long-term biochemical recurrence-free survival from pathologic stage data obtained at surgery or predicted from the Partin tables, along with surgical margin status and Gleason score information obtained at RRP.

Adenocarcinoma↗