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Peter R Carroll

Publications and source records attributed to Peter R Carroll.

At least 37 records · Page 2Linked to original sources
PubMed2006

Comorbidity and primary treatment for localized prostate cancer: data from CaPSURE.

PURPOSE: The optimal approach for treating localized prostate cancer remains controversial, leading to a multifactorial decision making process. We characterized the extent to which the presence and number of comorbidities affects treatment for localized prostate cancer. MATERIALS AND METHODS: Data were abstracted from a longitudinal observational database of men with prostate cancer. A total of 5,149 men diagnosed with localized prostate cancer between 1995 and 2001 were included in this analysis if they had been treated with RP, external beam radiation, brachytherapy, hormonal therapy or surveillance. Comorbidity was assessed through a patient reported checklist of conditions. Multinomial logistic regression was used to determine the OR of the likelihood of receiving each type of therapy. The number of comorbidities and specific comorbidities in patients receiving RP were compared with comorbidities in patients receiving other treatment. RESULTS: The adjusted OR showed a dose response between the number of comorbidities and an increasing probability of any nonRP treatment. In addition, heart disease, stroke or another urinary condition were found to be associated with treatment. CONCLUSIONS: Patient comorbidities affect decision making regarding treatment for localized prostate cancer. Urologists and other physicians treating this disease appear to evaluate patient comorbidities when selecting treatment options.

Aged↗
PubMed2006

Impact of increased number of biopsies on the nature of prostate cancer identified.

PURPOSE: Increasing the number of cores obtained at the time of transrectal ultrasound guided prostate biopsy has increased the number of cancers identified. However, there is increasing recognition that many men with prostate cancer may not benefit from early, aggressive intervention and that over detection of prostate cancer has resulted in over treatment. We determined the impact of the greater number of prostate biopsies on the nature of cancer identified. MATERIALS AND METHODS: In the Cancer of the Prostate Strategic Urologic Research Endeavor database, a longitudinal disease registry of men with prostate cancer, we identified those men diagnosed between 1999 and 2002 with complete data on serum prostate specific antigen, Gleason score, clinical T stage, number of biopsies obtained and number involved with cancer. RESULTS: We identified 4,072 men with 6 or more prostate biopsies obtained at initial diagnosis. Of the men 30%, 47% and 24% underwent 6, 7 to 11, and more than 12 biopsies, respectively. The number of biopsies correlated significantly with numerous sociodemographic and clinical variables including prostate specific antigen, comorbidities and income. There did not appear to be differences in disease characteristics as assessed by Kattan and Cancer of the Prostate Risk Assessment scores among men with a biopsy number between 6 and 17. In the subset of 1,548 men undergoing radical prostatectomy, no differences in biochemical-free survival were observed among the various biopsy groups at a median followup of 2.2 years. CONCLUSIONS: The increasing number of prostate biopsies obtained at diagnosis increases cancer detection but the impact on disease characteristics remains unclear. Our data suggest that the risk stratification of prostate cancers is independent of biopsy number (6 or greater) in a contemporary cohort of men.

Aged↗
PubMed2006

Laparoscopic versus open cytoreductive nephrectomy in advanced renal-cell carcinoma.

BACKGROUND AND PURPOSE: There is growing evidence of the benefit of cytoreductive nephrectomy prior to immunotherapy in patients with advanced renal-cell carcinoma (RCC). We compared the outcomes of patients with metastatic RCC undergoing laparoscopic and open cytoreductive nephrectomy prior to systemic therapy. PATIENTS AND METHODS: We retrospectively analyzed 27 patients undergoing cytoreductive nephrectomy for metastatic RCC between 2000 and 2004, 16 laparoscopically and 11 by an open approach. Patients with inferior vena-caval tumor thrombus were excluded from analysis. The two groups were comparable with regard to tumor size, clinical stage, and performance status. Surgical, pathologic, and perioperative characteristics and outcomes were compared. RESULTS: The laparoscopic technique was associated with reduced blood loss (149 v 1135 mL; P = 0.03), transfusion rate and quantity (13% v 55%; P = 0.03; 0.13 v 2.0 units of packed red blood cells; P = 0.007), shorter time to oral intake (1.2 v 2.7 days; P < 0.001), and shorter hospitalization (3.6 v 6.8 days; P < 0.001) compared with open nephrectomy. No significant differences were observed with respect to pathologic stage, operative time, complications, fraction receiving subsequent systemic therapy, time to systemic therapy, or survival. CONCLUSIONS: Laparoscopic cytoreductive nephrectomy is associated with reduced morbidity and hospital stay compared with open surgery. There was no increase in complications, and the ability to proceed with subsequent systemic therapy was maintained in the majority of patients. The laparoscopic approach can be considered in patients with metastatic RCC as part of a cytoreductive and systemic-therapy regimen.

Carcinoma, Renal Cell↗
PubMed2006

Prostate cancer: endorectal MR imaging and MR spectroscopic imaging--distinction of true-positive results from chance-detected lesions.

PURPOSE: To retrospectively investigate size criteria for the identification of chance-detected lesions at endorectal magnetic resonance (MR) imaging and MR spectroscopic imaging of prostate cancer. MATERIALS AND METHODS: Approval of the committee on human research and written informed consent were obtained. This study was HIPAA compliant. Endorectal MR imaging and MR spectroscopic imaging were performed with a 1.5-T MR imager in 48 men with a mean age of 59 years (age range, 47-75 years) prior to radical prostatectomy. Two independent readers recorded the size and location of all suspected peripheral zone tumor nodules on MR images alone and on images obtained with combined MR imaging and MR spectroscopic imaging. Nodules detected at MR imaging were classified as matched lesions if tumor was present in the same location at step-section histopathologic review. For all matched lesions, kappa values were calculated to examine agreement between measured and actual tumor size. Lesions that were overmeasured at MR imaging with a kappa value of less than 0.2 were considered chance-detected lesions. RESULTS: At MR imaging, two of 27 and four of 35 matched lesions for readers 1 and 2, respectively, were chance-detected lesions. The corresponding numbers of lesions at combined MR imaging and MR spectroscopic imaging were one of 21 and one of 31, respectively. In all but two cases, the measured diameter of chance-detected lesions was more than twice that of the diameter at histopathologic analysis. By using this diameter threshold to distinguish true-positive results, the mean diameter of detected tumors at histopathologic analysis was 15 mm compared with 4 mm for both undetected and chance-detected tumors (P < .05). CONCLUSION: To ensure uniformity in the comparison of scientific studies, peripheral zone tumors detected at MR imaging and MR spectroscopic imaging of the prostate that are in the same location as tumors detected at histopathologic review should be considered chance-detected lesions if the MR transverse diameter is more than twice the histopathologic transverse diameter.

Aged↗
PubMed2006

Genomic profiling of hormone-naïve lymph node metastases in patients with prostate cancer.

The progression of organ-confined prostate cancer to metastatic cancer is inevitably fatal. Consequently, identification of structural changes in the genome and associated transcriptional responses that drive this progression is critical to understanding the disease process and the development of biomarkers and therapeutic targets. In this study, whole genome copy number changes in genomes of hormone-naïve lymph node metastases were profiled using array comparative genomic hybridization, and matched primaries were included for a subset. Matched primaries and lymph node metastases showed very similar copy number profiles that are distinct from primary tumors that fail to metastasize.

Biomarkers, Tumor↗
PubMed2006

Magnetic resonance imaging and spectroscopy of prostate cancer.

Magnetic resonance imaging may improve the staging of prostate cancer compared with clinical evaluation alone, computerized tomography, or transrectal ultrasound, and it allows simultaneous and detailed evaluation of prostatic, periprostatic, and pelvic anatomy. Endorectal magnetic resonance imaging and magnetic resonance spectroscopic imaging (endoMRI/MRSI) allow better visualization of the zonal anatomy of the prostate and better delineation of tumor location, volume, and extent (stage). Metabolic criteria used to identify and localize prostate cancer with endoMRI/MRSI have been standardized, thus improving the accuracy of the examination and limiting interobserver variations in interpretation. Evidence is now emerging that endoMRI/MRSI may also be helpful in assessing response to prostate cancer treatment, most commonly with radiation and/or androgen-deprivation therapy.

Journal Article↗
PubMed2005

The changing face of prostate cancer.

Prostate cancer remains the most common noncutaneous human malignancy, and the second most lethal tumor among men. However, the natural history of the disease is often prolonged, and the survival benefits of local therapy for men with low-risk tumors may not be realized for a decade or more, as is increasingly well demonstrated in long-term observational cohorts in both the United States and Europe. A significant proportion of men with prostate cancer may be overdiagnosed, in the sense that diagnosis may not improve their lifespan or quality of life. However, the extent to which overdiagnosis represents a true problem relates to the consistency with which diagnosis leads invariably to active treatment. Prostate cancer is diagnosed at progressively earlier stages and with lower risk features; despite these trends, patients are less likely now than a decade ago to undergo a trial of active surveillance. Rates of brachytherapy and hormonal therapy use, in particular, have risen markedly. Important progress has been made in recent years in prostate cancer risk assessment. These advances, in combination with biomarkers in later stages of development, should be expected in the coming years to yield further improvements in clinicians' ability to diagnose prostate cancer early, and guide appropriately selected patients toward increasingly tailored treatment.

Humans↗
PubMed2005

Promoter CpG hypomethylation and transcription factor EGR1 hyperactivate heparanase expression in bladder cancer.

Heparanase plays a critical role in the degradation of extracellular matrix and cell membrane and is frequently upregulated in malignant tumors. Transcription factor, early growth response 1 (EGR1), is closely associated with inducible transcription of the heparanase gene. We hypothesized that promoter CpG hypomethylation with increased EGR1 expression could determine heparanase expression during the pathogenesis of bladder cancer. Bladder cancer cell lines (J82, T24 and transitional cell carcinoma) significantly restored heparanase expression after 5-Aza-dC treatment. Transfection of EGR1 siRNA with T24 bladder cancer cell line significantly downregulated heparanase expression compared to the control siRNA transfection. In 54 bladder cancer and paired normal bladder samples, heparanase expression was significantly higher in bladder cancer than in normal bladder (P<0.01). We performed methylation-specific PCR targeting the CpG sites within the core-binding consensus motifs of EGR1 (GGCG) and Sp1 (GGGCGG). Methylation prevalence was significantly higher in normal bladder than in bladder cancer (P<0.05) and inversely correlated with heparanase expression (P=0.055). In the total series of bladder cancer and normal bladder samples, the combination of promoter CpG methylation and EGR1 expression regulated heparanase expression in a stepwise manner, where heparanase expression was the lowest in methylation-positive and EGR1-negative samples and the highest in methylation-negative and EGR1-positive samples. To our knowledge, this is the first study demonstrating that increased heparanase expression during the pathogenesis of bladder cancer is due to promoter hypomethylation and transcription factor EGR1.

Base Sequence↗
PubMed2005

Predictors of prostate cancer-specific mortality after radical prostatectomy or radiation therapy.

PURPOSE: We evaluated predictors of prostate cancer-specific mortality (PCSM) after prostate-specific antigen (PSA) failure after radical prostatectomy (RP) or radiation therapy (RT). PATIENTS AND METHODS: A total of 1,159 men with clinically localized prostate cancer treated with RP (n = 498) or RT (n = 661) developed PSA failure, and they formed the study cohort. Competing risk regression analyses were used to evaluate whether previously identified predictors of time to metastasis, including post-treatment PSA doubling time (PSA-DT), Gleason score, and interval to PSA failure, could also predict time to PCSM after PSA failure. The cumulative incidence method was used to estimate PCSM after PSA failure. RESULTS: A post-RP PSA-DT of less than 3 months (hazard ratio [HR], 54.9; 95% CI, 16.7 to 180), a post-RT PSA-DT of less than 3 months (HR, 12.8; 95% CI, 7.0 to 23.1), and a biopsy Gleason score of 8 to 10 (HR, 6.1; 95% CI, 3.4 to 10.7) for patients treated with RT were significantly associated with PCSM. Post-RP estimated rates of PCSM 5 years after PSA failure were 31% (95% CI, 17% to 45%) v 1% (95% CI, 0% to 2%) for patients with PSA-DT of less than 3 months v > or = 3 months. Post-RT estimated rates of PCSM 5 years after PSA failure were 75% (95% CI, 59% to 92%) v 35% (95% CI, 24% to 47%) for patients with a biopsy Gleason score of > or = 8 v < or = 7, respectively, and PSA-DT of less than 3 months; these rates were 15% (95% CI, 0.8% to 28%) v 4% (95% CI, 1% to 6%), respectively, for patients with a PSA-DT > or = 3 months. CONCLUSION: Patients at high risk for PCSM after PSA failure can be identified based on post-RP PSA-DT or post-RT PSA-DT and biopsy Gleason score. These parameters may be useful in identifying patients for a randomized trial evaluating hormonal therapy with or without docetaxel.

Aged↗
PubMed2005

Prostate-specific antigen nadir and cancer-specific mortality following hormonal therapy for prostate-specific antigen failure.

PURPOSE: For men receiving androgen-suppression therapy (AST) for a rising postoperative or postradiation prostate-specific antigen (PSA), we evaluated whether a PSA nadir of more than 0.2 ng/mL was significantly associated with prostate cancer-specific mortality (PCSM). PATIENTS AND METHODS: The study cohort comprised 747 men with rising PSA and negative bone scan after surgery (n = 486) or radiation therapy (n = 261) who were treated with AST. Cox regression was used to evaluate whether a significant association existed between the PSA nadir level after 8 months of AST and the time to PCSM, controlling for treatment and known prognostic factors. RESULTS: The post-AST PSA nadir (pCox < .0001), the pre-AST PSA doubling time (DT) (pCox = .002), PSA level (P = .0001), and Gleason eight to 10 cancers (pCox = .01) were significantly associated with time to PCSM. The adjusted hazard ratio for PCSM was 20 (95% CI, 7 to 61; pCox < .0001), for men with a PSA nadir of more than 0.2 ng/mL as compared with all others. A PSA DT of less than 3 months was observed in 30% (224 of 747) of the study cohort. Of the 28 observed prostate cancer deaths, 21 (75%) occurred in men whose PSA nadir was more than 0.2 ng/mL and who had a PSA DT of less than 3 months. CONCLUSION: A PSA nadir of more than 0.2 ng/mL after 8 months of AST given for postoperative or postradiation PSA failure is significantly associated with PCSM and is clinically significant because it accounted for 75% of the cancer deaths observed in this study.

Aged↗
PubMed2005

Multigene methylation analysis for detection and staging of prostate cancer.

PURPOSE: Aberrant gene promoter methylation profiles have been well-studied in human prostate cancer. Therefore, we rationalize that multigene methylation analysis could be useful as a diagnostic biomarker. We hypothesize that a new method of multigene methylation analysis could be a good diagnostic and staging biomarker for prostate cancer. EXPERIMENTAL DESIGN: To test our hypothesis, prostate cancer samples (170) and benign prostatic hyperplasia samples (69) were examined by methylation-specific PCR for three genes: adenomatous polyposis coli (APC), glutathione S-transferase pi (GSTP1), and multidrug resistance 1 (MDR1). The methylation status of representative samples was confirmed by bisulfite DNA sequencing analysis. We further investigated whether methylation score (M score) can be used as a diagnostic and staging biomarker for prostate cancer. The M score of each sample was calculated as the sum of the corresponding log hazard ratio coefficients derived from multivariate logistic regression analysis of methylation status of various genes for benign prostatic hyperplasia and prostate cancer. The optimal sensitivity and specificity of the M score for diagnosis and for staging of prostate cancer was determined by receiver-operator characteristic (ROC) curve analysis. A pairwise comparison was employed to test for significance using the area under the ROC curve analysis. For each clinicopathologic finding, the association with prostate-specific antigen (PSA) failure-free probability was determined using Kaplan-Meier curves and a log-rank test was used to determine significance. The relationship between M score and clinicopathologic findings was analyzed by either the Mann-Whitney U test, Kruskal-Wallis test, or the Spearman rank correlation test. RESULTS: The frequency of positive methylation-specific PCR bands for APC, GSTP1, and MDR1 genes in prostate cancer samples was 64.1%, 54.0%, and 55.3%, respectively. In benign prostatic hyperplasia samples, it was 8.7%, 5.8%, and 11.6%, respectively. There was a significant correlation of M score with high pT category (P < 0.001), high Gleason sum (P < 0.001), high preoperative PSA (P = 0.027), and advanced pathologic features. For all patients, the M score had a sensitivity of 75.9% and a specificity of 84.1% as a diagnostic biomarker using a cutoff value of 1.0. In patients with low or borderline PSA levels (<10.0 ng/mL), the M score was significantly higher in prostate cancers than in benign prostatic hyperplasias (2.635 +/- 0.200 and 0.357 +/- 0.121, respectively). ROC curve analysis revealed that the M score had a sensitivity of 65.4% and a specificity of 94.2% when 1.0 was used as a cutoff value. For all patients, M score can distinguish organ-confined (< or =pT(2)) from locally advanced cancer (> or =pT(3)) with a sensitivity of 72.1% and a specificity of 67.8%. Moreover, considering patients with PSA levels of <10 ng/mL, the M score has a sensitivity of 67.1% and a specificity of 85.7%. The ROC curve analysis showed a significant difference between M score and PSA (P = 0.010). CONCLUSIONS: This is the first report demonstrating that M score is a new method for multigene methylation analysis that can serve as a good diagnostic and staging biomarker for prostate cancer.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Ethnic group-related differences in CpG hypermethylation of the GSTP1 gene promoter among African-American, Caucasian and Asian patients with prostate cancer.

The incidence and mortality of prostate cancer (PC) is approximately 2-fold higher among African-Americans as compared to Caucasians and very low in Asian. We hypothesize that inactivation of GSTP1 genes through CpG methylation plays a role in the pathogenesis of PC, and its ability to serve as a diagnostic marker that differs among ethnic groups. GSTP1 promoter hypermethylation and its correlation with clinico-pathological findings were evaluated in 291 PC (Asian = 170; African-American = 44; Caucasian = 77) and 172 benign prostate hypertrophy samples (BPH) (Asian = 96; African-American = 38; Caucasian = 38) using methylation-specific PCR. In PC cells, 5-aza-dC treatment increased expression of GSTP1 mRNA transcripts. The methylation of all CpG sites was found in 191 of 291 PC (65.6%), but only in 34 of 139 BPH (24.5%). The GSTP1 hypermethylation was significantly higher in PC as compared to BPH in each ethnic group (p < 0.0001). Logistic regression analysis (PC vs. BPH) showed that African-Americans had a higher hazard ratio (HR) (13.361) compared to Caucasians (3.829) and Asian (8.603). Chi-square analysis showed correlation of GSTP1 hypermethylation with pathological findings (pT categories and higher Gleason sum) in Asian PC (p < 0.0001) but not in African-Americans and Caucasian PC. Our results suggest that GSTP1 hypermethylation is a sensitive biomarker in African-Americans as compared to that in Caucasians or Asian, and that it strongly influences tumor progression in Asian PC. Ours is the first study investigating GSTP1 methylation differences in PC among African-American, Caucasian and Asian.

Adult↗
PubMed2005

Functional Loss of the gamma-catenin gene through epigenetic and genetic pathways in human prostate cancer.

Gamma-catenin is a cell adhesion molecule and a candidate mediator of Wnt signal transduction. We hypothesized that impaired regulation of gamma-catenin through genetic and epigenetic pathways is associated with the pathogenesis of prostate cancer. To test this hypothesis, cytosine-phosphate-guanine methylation, loss of heterozygosity (LOH), and mutation status of the gamma-catenin gene were analyzed in cultured prostate cancer cell lines, 180 localized prostate cancers, 69 benign prostatic hyperplasias, and 11 hormone refractory prostate cancers (HRPC). In prostate cancer cell lines (DuPro, LNCaP, ND-1, and PC3), gamma-catenin mRNA transcripts were increased after 5-aza-2'-deoxycytidine treatment. In localized prostate cancer, gamma-catenin expression was lower but prevalence of gamma-catenin methylation was higher compared with benign prostatic hyperplasia. However, gamma-catenin methylation did not correlate with Gleason sum, pT category, or capsular penetration. Among localized prostate cancers with positive gamma-catenin methylation, the presence of LOH at chromosome 17q21 was closely related to down-regulation of gamma-catenin mRNA expression. The gamma-catenin mutations were not found in localized prostate cancers, whereas six mutations were found in five HRPCs within or close to the GSK-3beta consensus motif phosphorylation site, among which four HRPCs showed strong nuclear gamma-catenin accumulation. In these four HRPCs, Bcl-2 expression was increased, whereas the target of the Wnt signal, c-myc, was only expressed in one HRPC. Therefore, although epigenetic gamma-catenin methylation is an early event in the development of prostate cancer, simultaneous events of epigenetic cytosine-phosphate-guanine methylation and genetic LOH may be responsible for functional loss of gamma-catenin. The gamma-catenin mutation related to Bcl-2 overexpression has a significant effect on the pathogenesis of HRPC. This is the first report to characterize the epigenetic and genetic regulation of gamma-catenin in human prostate cancer.

Amino Acid Sequence↗
PubMed2005

Epigenetic changes in prostate cancer: implication for diagnosis and treatment.

Prostate cancer is the most common noncutaneous malignancy and the second leading cause of cancer death among men in the United States. DNA methylation and histone modifications are important epigenetic mechanisms of gene regulation and play essential roles both independently and cooperatively in tumor initiation and progression. Aberrant epigenetic events such as DNA hypo- and hypermethylation and altered histone acetylation have both been observed in prostate cancer, in which they affect a large number of genes. Although the list of aberrantly epigenetically regulated genes continues to grow, only a few genes have, so far, given promising results as potential tumor biomarkers for early diagnosis and risk assessment of prostate cancer. Thus, large-scale screening of aberrant epigenetic events such as DNA hypermethylation is needed to identify prostate cancer-specific epigenetic fingerprints. The reversibility of epigenetic aberrations has made them attractive targets for cancer treatment with modulators that demethylate DNA and inhibit histone deacetylases, leading to reactivation of silenced genes. More studies into the mechanism and consequence of demethylation are required before the cancer epigenome can be safely manipulated with therapeutics as a treatment modality. In this review, we examine the current literature on epigenetic changes in prostate cancer and discuss the clinical potential of cancer epigenetics for the diagnosis and treatment of this disease.

Acyltransferases↗
PubMed2005

Methylation of the gamma-catenin gene is associated with poor prognosis of renal cell carcinoma.

PURPOSE: Gamma-catenin is a cell adhesion protein, and its functional loss is associated with tumor invasion and metastasis. We hypothesize that (1) promoter CpG methylation regulates the expression and function of the gamma-catenin gene in renal cell carcinoma (RCC) and (2) methylation of the gamma-catenin gene is associated with poor prognosis of RCC. To test these hypotheses, we analyzed the CpG methylation status of the gamma-catenin gene and its correlation with clinical outcome in RCC. EXPERIMENTAL DESIGN: Genomic DNA and total RNA were extracted from three renal cancer cell lines (A498, Caki-1, and Caki-2) and 54 RCC tissue samples with their corresponding normal kidney tissue samples. Expression of gamma-catenin gene was analyzed by reverse transcription-PCR and immunostaining. Promoter methylation was analyzed by two different methylation-specific PCR (MSP-A and MSP-B), and the results were verified by DNA sequencing. RESULTS: The demethylating agent (5-aza-2'-deoxycytidine) increased levels of mRNA transcript of the gamma-catenin gene in three renal cancer cell lines. Gamma-catenin mRNA and protein expression were significantly reduced in RCC samples compared with normal kidney samples, respectively (P < 0.05). MSP-A and MSP-B bands were detected in 45 of 54 (83.3%) and 49 of 54 (90.7%) RCC samples, respectively. In normal kidney, weak products of MSP-A and MSP-B were detected in 5 of 54 (9.3%) and 6 of 54 (11.1%) samples, respectively. Likewise, both MSP-A and MSP-B ratios were significantly higher in RCC samples compared with normal kidney samples, respectively (P < 0.01). Multivariate analysis revealed that the MSP-B ratio was a powerful and independent predictor superior to nuclear grade and Robson stage with respect to survival and disease progression (P = 0.029 and 0.0071, respectively). No mutations in the NH(2)-terminal region of gamma-catenin were found in this study. CONCLUSION: Expression of gamma-catenin is regulated by promoter CpG methylation, and the balance between methylated and unmethylated RCC cell populations could determine its functional role. Because the conventional nuclear grade and/or staging system have some limitations to predict precise clinical outcome, this is the first report demonstrating that promoter CpG methylation of gamma-catenin can be an independent and superior predictor for survival and disease progression.

Adult↗
PubMed2005

Multidisciplinary management of advanced prostate cancer: changing perspectives on referring patients and enhancing collaboration between oncologists and urologists in clinical trials.

Prostate cancer traditionally was managed by monotherapy, and treatment was almost exclusively provided by the urologic surgeon. As ongoing clinical trials in advanced disease identify novel agents or combination therapies with good tolerability and potential survival benefits, multidisciplinary management may offer optimal care for men with high-risk prostate cancer, as it does for women with breast cancer. Patients with high-risk recurrent or metastatic disease should be informed of clinical trials for which they may be eligible.

Aged↗
PubMed2005

Impact of obesity on prostate cancer recurrence after radical prostatectomy: data from CaPSURE.

OBJECTIVES: To determine the association between obesity and prostate cancer recurrence after primary treatment with radical prostatectomy. METHODS: Data were abstracted from CaPSURE, a disease registry of 10,018 men with prostate cancer. We included 2131 men who had undergone radical prostatectomy between 1989 and 2003 and had body mass index (BMI) information available. Recurrence was defined as two consecutive prostate-specific antigen (PSA) levels of 0.2 ng/mL or greater or any second treatment. Patients were risk stratified using the PSA level, Gleason grade, and clinical T stage. RESULTS: Patients were followed up for a median of 23 months. Of the 2131 patients, 251 (12%) developed recurrence at a median of 13 months (range 1 to 107); 183 (9%) of these men had PSA failure and 68 (3%) received a second treatment. After adjusting for risk group, ethnicity, age, and comorbidities, a significant association was found between an increasing BMI and disease recurrence (P = 0.028). Very obese patients (BMI 35 kg/m2 or more) were 1.69 times more likely to have recurrence relative to men of normal weight (BMI less than 25.0 kg/m2; 95% confidence interval [CI] 1.01 to 2.84). An increasing PSA level (P <0.0001) and Gleason grade (P <0.0001) were also associated with recurrence. Ethnicity was not significantly associated with either BMI or PSA recurrence (P = 0.685 and P = 0.068, respectively). CONCLUSIONS: The results of our study have shown that obesity is an independent predictor of prostate cancer recurrence. Because of the increased comorbidities and greater rates of recurrence, obese individuals undergoing radical prostatectomy need vigilant follow-up care.

Adult↗