ObjetivosRecientemente, el Estudio Aleatorizado Europeo de Screening del Cáncer de Próstata consiguió una reducción de la mortalidad por cáncer de próstata mediante la determinación sérica de antígeno específico-prostático (PSA). Estos resultados no fueron reproducidos en la rama española del Estudio Aleatorizado Europeo de Screening del Cáncer de Próstata. La contaminación de PSA (determinación oportunista fuera del estudio) podría disminuir el poder de contraste del estudio si se lleva a cabo en el brazo control. Hemos calculado la tasa de contaminación de PSA a largo plazo, y su efecto en la realización de biopsia prostática y en la detección de cáncer.Material y métodosSe aleatorizaron 4.276 varones (2.415 brazo screening, 1.861 brazo control) en la sección española del Estudio Aleatorizado Europeo de Screening del Cáncer de Próstata. No se programó la determinación de PSA en el brazo control. Se indicó biopsia prostática sextante si PSA≥3ng/ml. Toda determinación de PSA realizada fuera del estudio fue etiquetada como «contaminación de PSA». Se calcularon las tasas de contaminación de PSA, realización de biopsia y detección de cáncer.ResultadosLas medianas de edad y tiempo de seguimiento fueron de 57 y 15,1 años respectivamente. Un total de 2.511 varones se realizó al menos una determinación de PSA fuera del estudio. La contaminación de PSA a los 5, 10 y 15 años fue del 22; 47,1 y 66,3% en el brazo screening, y del 20,8; 43,2 y 58,6 en el brazo control, respectivamente (p<0,0001). La tasa de biopsia a los 5, 10 y 15 años fue del 19,3; 22,6 y 24,1% (screening) y del 1; 3,6 y 7,1% (control), respectivamente (p<0,0001). La detección de cáncer de próstata fue del 6,7% (screening) y del 4,3% (control, p=0,0006).ConclusionesAunque la contaminación acumulada de PSA fue notable en los 2 brazos del estudio, la realización de biopsia prostática fue escasa en el brazo control. Por ello, creemos que el impacto de la contaminación de PSA sobre el poder estadístico del estudio debe ser limitado.

Objectives: Recently, the European Randomized Study of Screening for Prostate Cancer achieved a reduction in prostate cancer mortality by measuring serum prostate-specific antigen (PSA) levels. These results were not reproduced in the Spanish arm of European Randomized Study of Screening for Prostate Cancer. PSA contamination (opportunistic measurements outside the study) could decrease the study's contrasting power if performed in the control arm. We have calculated the long-term rate of PSA contamination and its effect on performing prostate biopsy and detecting cancer.Material and methods: A total of 4,276 men were randomised (2,415 to the screening arm, 1,861 to the control arm) in the Spanish section of the European Randomized Study of Screening for Prostate Cancer. PSA measurements were not scheduled in the control arm. Sextant prostate biopsy was indicated if PSA levels were >= 3 ng/mL. All PSA readings performed outside the study were labelled as "PSA contamination". We calculated the rates of PSA contamination, biopsy implementation and cancer detection.Results: The median age and follow-up time were 57 and 15.1 years, respectively. A total of 2,511 men underwent at least one PSA reading outside the study. PSA contamination at 5, 10 and 15 years was 22.0%, 47.1% and 66.3% in the screening arm, respectively, and 20.8%, 43.2% and 58.6% in the control arm, respectively (P<.0001). The biopsy rate at 5, 10 and 15 years was 19.3%, 22.6% and 24.1% (screening), respectively, and 1.0%, 3.6% and 7.1% (control), respectively (P<.0001). The PC detection rate was 6.7% (screening) and 4.3% (control; P=.0006).Conclusions: Although the cumulative PSA contamination was pronounced in the 2 study arms, the rate of prostate biopsies was low in the control arm. We therefore believe that the effect of PSA contamination on the study's statistical power should be limited. (C) 2015 AEU. Published by Elsevier Espana, S.L.U. All rights reserved.

Objetivo En la actualidad el papel del screening del cáncer de próstata (CaP) está cuestionado. El estudio aleatorizado europeo de screening del cáncer de próstata (ERSPC) tiene como objetivo demostrar si el screening del CaP reduce la mortalidad por esta enfermedad. Se muestran los resultados en la rama española de este estudio: mortalidad global y cáncer-específica, características de los tumores detectados, de los tratamientos primarios y de la progresión a enfermedad avanzada. Material y métodos Se invitó a participar a 18.612 varones entre los 45 y 70 años de edad, excluyendo aquellos con una expectativa de vida inferior a 10 años. Se llevó a cabo aleatorización a brazo screening (determinación de PSA sérico) y brazo control (no pruebas diagnósticas). Se indicó biopsia prostática aleatorizada sextante dirigida por ecografía transrectal en los varones del brazo screening con PSA≥3ng/ml. Se identificaron los CaP detectados (estadio y tratamiento primarios), así como los fallecimientos producidos (fecha y causa de la muerte). Resultados El estudio se llevó a cabo con 4.276 varones (2.415 brazo screening, 1.861 brazo control). Las medianas de edad y PSA sérico fueron de 57 años y 0,90ng/ml respectivamente. El tiempo de seguimiento (mediana) fue de 15,8 años. Se diagnosticaron 242 CaP, 162 (6,7%) en el brazo screening y 80 (4,3%) en el control (p<0,001). De ellos 214 (88,4%) comenzaron con estadio clínico organoconfinado (91,4% brazo screening vs 82,5% control, p=0,024). Un total de 112 pacientes (46,3%) fue sometido a prostatectomía radical, 53 (21,9%) a radioterapia prostática, 24 (9,9%) a tratamiento hormonal y 47 (19,4%) a observación. Un total de 18 CaP evolucionaron a enfermedad avanzada (M+ o PSA>100ng/ml), sin diferencia entre los brazos del estudio (p=0,938). Un total de 618 (14,5%) fallecieron a lo largo del seguimiento: 340 (14,1%) en el brazo screening y 278 (14,9%) en el control, sin diferencias entre brazos en términos de mortalidad cáncer-específica (p=0,907) ni por todas las causas (p=0,399). Las principales causas de muerte encontradas fueron neoplasia (54,0%), cardiovascular (17,6%), respiratoria (8,7%) y digestiva (4,0%), sin diferencia entre brazos. De los 334 pacientes fallecidos por neoplasia tan solo 12 (3,6%) murieron por CaP. Conclusiones El screening del CaP produce una migración del diagnóstico hacia estadios más precoces. No obstante, no hemos demostrado un beneficio en términos de supervivencia global ni cáncer-específica tras más de 15 años de seguimiento. La baja mortalidad por esta enfermedad en nuestro entorno podría ser uno de los principales factores para explicar estos resultados.

Objective: The role of prostate cancer (PC) screening is currently being questioned. The objective of the European Randomized Study of Screening for Prostate Cancer (ERSPC) was to demonstrate whether PC screening reduced mortality from this disease. The results from the Spanish branch of this study are presented: all-cause and cancer-specific mortality, the characteristics of the detected tumors, primary treatments and progression to advanced disease.Material and methods: A total of 18,612 men, between the ages of 45 and 70, were invited to participate in the study, excluding those with a Life expectancy of less than 10 years. The men were randomized to the screening arm (serum prostate-specific antigen [PSA] reading) or the control arm (no diagnostic tests). Randomized transrectal ultrasound-guided sextant prostate biopsies were indicated for the men in the screening arm with PSA levels >= 3 ng/ml. The detected PCs were identified (stage and primary treatment), as well as the deaths that occurred (date and cause of death).Results: The study was performed with 4276 men (2415 in the screening arm and 1861 in the control arm). The median age and serum PSA level were 57 years and 0.90 ng/mL, respectively. The median follow-up time was 15.8 years. A total of 242 PCs were diagnosed, 162 (6.7%) in the screening arm and 80 (4.3%) in the control arm (P<.001). Of these, 214 (88.4%) had an organ-confined clinical stage at onset (91.4% in the screening arm vs. 82.5% in the control arm; P=.024). A total of 112 patients (46.3%) underwent radical prostatectomy, 53 (21.9%) underwent prostate radiation therapy, 24 (9.9%) underwent hormone therapy and 47 (19.4%) were kept under observation. A total of 18 PCs progressed to advanced disease (M+ or PSA levels > 100 ng/mL), with no differences between the study arms (P=.938). A total of 618 (14.5%) patients died during follow-up: 340 (14.1%) in the screening arm and 278 (14.9%) in the control arm, with no differences between the arms in terms of cancer-specific (P=.907) or all-cause (P=.399) mortality. The main causes of death were neoplasia (54.0%), cardiovascular (17.6%), respiratory (8.7%) and gastrointestinal (4.0%), with no difference between study arms. Of the 334 patients who died from neoplasia, only 12 (3.6%) died from PC.Conclusions: PC screening results in a shifting of the diagnosis towards earlier stages. Nevertheless, we have not demonstrated a benefit in terms of overall or cancer-specific survival after more than 15 years of follow-up. The low mortality from this disease in our community could be one of the main factors that explain these results. (C) 2014 AEU. Published by Elsevier Espana, S.L.U. All rights reserved.

BACKGROUND: To present the long-term results of a prostate cancer (PC) screening trial conducted in a Mediterranean setting. METHODS: A total of 4276 men aged 45–70 years were randomized to screening arm (PSA test performed) and control arm (no tests). Transrectal ultrasonography-guided sextant prostate biopsy was conducted when PSA⩾3 ng ml −1 . Date and cause of death were retrieved from death certificates. PC incidence, and disease-specific and overall mortality curves were plotted and comparison between arms was made. Analysis of causes of death was also performed. RESULTS: Median age at randomization was 57.0 years. Median follow-up time was 15.2 years. A total of 241 men were diagnosed with PC, 161 (6.7%) in the screening arm and 80 (4.3%) in the control arm ( P <0.01). Eventually, 554 men (13%) died. No difference in all-cause mortality was found between arms ( P =0.34). Only 10 men (10/4276, 0.23%) died from PC, no differences between arms ( P =0.67). Overall, the main causes of death were malignancy (54.2%), cardiovascular (17.9%) and respiratory (9.2%) diseases. Main cancer causes of death were lung and bronchus cancer (37.2%), colorectum (15.0%) and stomach (9.0%) cancer. PC only accounted for 3.0% of all malignant causes of death (ranked 10th). CONCLUSIONS: Our study failed to demonstrate benefits of PC screening in terms of all-cause and PC-specific mortality after a median follow-up of 15 years. The limited sample size and the low long-term PC mortality observed in our setting were probably the most important factors to explain these results.

Objective: To address if prostate cancer (PCa) screening decreases PCa mortality in the asymptomatic population, within the setting of the Spanish arm of the European Randomized Study of Screening for Prostate Cancer (ERSPC).Material and methods: From 1996 to 1999, 4,278 men aged 45-70 years were recruited and randomized to the screening arm (PSA every 4 years, prostate biopsy when PSA >= 3 ng/ml) and control arm (no tests). Dates and causes of death were collected on an annual basis. A Kaplan-Meier analysis was used to calculate overall and cancer-specific survival.Results: A total of 2,416 men were recruited in the screening arm and 1,862 in the control arm. Mean age was 57.8 years, median follow-up was 13.3 years. At the end of the follow-up period, 427 deaths (9 from PCa) were observed. Survival analysis did not show any difference between the study arms with respect to overall and cancer-specific survival (p = 0.939 and p = 0.544 respectively). Most relevant causes of death were malignant tumors (52.9%), cardiovascular disease (17.3%) and respiratory (8.9%). Only 2.1% of deaths (0.2% of all recruited men) were due to PCa (2.5% screening, 1.6% control).Conclusions: The Spanish arm of ERSPC failed to reproduce the long-term results shown in the whole study. No differences in mortality (overall or cancer-specific) were observed after 15 years of follow-up. PCa mortality was infrequent (less than 1%). These results suggest limited yield of PCa screening in our setting. (C) 2011 AEU. Published by Elsevier Espana, S.L. All rights reserved.

ObjetivoEstudiar si el screening del cáncer de próstata (CaP) reduce la mortalidad por esta enfermedad en la población asintomática, dentro del ámbito de la rama española del European Randomized Study of Screening for Prostate Cancer (ERSPC).Material y métodosEntre 1996 y 1999 fueron reclutados 4.278 varones con edades comprendidas entre los 45 y los 70 años. Fueron aleatorizados a brazo screening (PSA cada 4 años, con biopsia prostática si PSA≥3ng/ml) y brazo control (no tests). De modo anual se registraron fechas y causas de mortalidad. Se realizó un análisis Kaplan-Meier para calcular la supervivencia global y cáncer-específica.ResultadosSe reclutaron 2.416 sujetos en el brazo screening y 1.862 en el control. La edad media fue de 57,8 años y la mediana del tiempo de seguimiento de 13,3 años. Al finalizar el seguimiento se registraron 427 fallecimientos (9 por CaP). El análisis de supervivencia no mostró diferencia entre los brazos del estudio con respecto a la mortalidad global ni cáncer-específica (p=0,939 y p=0,544 respectivamente). Las causas principales de muerte fueron los tumores malignos (52,9%), las enfermedades cardiovasculares (17,3%) y respiratorias (8,9%). Solo un 2,1% de las muertes (0,2% de todos los reclutados) fueron causadas por CaP (2,5% screening, 1,6% control).ConclusionesLa rama española del ERSPC no ha reproducido los resultados a largo plazo del estudio principal, no observándose diferencias en la mortalidad (global o cáncer-específica) después de 15 años de seguimiento. La mortalidad por CaP fue muy limitada (inferior al 1%). Estos resultados apoyan el escaso rendimiento del screening del CaP en nuestro entorno.

You have accessJournal of UrologyDiscussed Poster, Sunday, May 21, 2006, 1:00 - 4:00 pm1 Apr 2006421: Effects of Wine Polyphenols on the Expression of Ciclooxygenase-2 and Apoptosis in Androgen-Independent PC-3 Cell Line Antonio Ferruelo, Ignacio Romero, Antonio Berenguer, and Javier C. Angulo Antonio FerrueloAntonio Ferruelo More articles by this author , Ignacio RomeroIgnacio Romero More articles by this author , Antonio BerenguerAntonio Berenguer More articles by this author , and Javier C. AnguloJavier C. Angulo More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(18)32677-6AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "421: Effects of Wine Polyphenols on the Expression of Ciclooxygenase-2 and Apoptosis in Androgen-Independent PC-3 Cell Line." The Journal of Urology, 175(4S), p. 137 © 2016 by American Urological AssociationFiguresReferencesRelatedDetails Volume 175Issue 4SApril 2006Page: 137 Advertisement Copyright & Permissions© 2016 by American Urological AssociationMetricsAuthor Information Antonio Ferruelo More articles by this author Ignacio Romero More articles by this author Antonio Berenguer More articles by this author Javier C. Angulo More articles by this author Expand All Advertisement PDF downloadLoading ...

Objective: To evaluate the clinical utility of using the real-time reverse transcriptase-polymerase chain reaction (RT-PCR) to quantify prostate-specific antigen (PSA) mRNA in peripheral blood samples from patients with prostate cancer as a predictor of extraprostatic extension of the disease and to assess any correlations with known predictive markers of this condition. Methods: Immediately before radical prostatectomy, peripheral blood samples were taken from 42 men with clinically localized prostate cancer and analysed for PSA and 18S ribosomal (endogenous control) genes using real-time RT-PCR (with gene expression assays and the comparative CT–cycle threshold—method for quantifing). A total of 30 healthy male blood donors aged <50 y was taken as a control group.The relationships between PSA mRNA values, pathological and clinical features were analysed. PSA mRNA value, PSA level and biopsy Gleason score were then compared as predictors of extraprostatic extension. Results: PSA gene expresion was 3.73 times significantly higher in patients with clinically localized prostate cancer than in healthy men (P<0.05). There was no relationship between PSA real-time RT-PCR values and pathological stage pT2 or pT3 (P=0.5), and no association between PSA mRNA value and serum PSA level (P=0.9) or the Gleason score of the preoperative biopsy (P=0.9). Conclusion: There was no significant advantage in using the real-time RT-PCR assay of PSA mRNA before surgery to stage prostate cancer and to discriminate between organ-confined and extraprostatic extension.

OBJECTIVETo validate the spontaneous hypertensive rat (SHR) model for basic research into benign prostate hyperplasia (BPH), and to assess doxazosin‐induced changes in prostatic structure and apoptotic status.MATERIALS AND METHODSFour groups of rats were assessed: group 1, 15 SHRs treated with doxazosin; group 2, 14 SHRs with unilateral excision of the major pelvic ganglion; group 3, 14 untreated SHRs; and group 4, 16 intact Wistar‐Kyoto (WKY) rats. The doxazosin mesylate (0.03 mg daily) was given compacted in rat food for 3 months. The prostatic ventral lobe (VL) was excised and weighed. Stereological light microscopy, multiplex reverse transcription‐polymerase chain reaction of prostate caspases, and caspase‐3 activity (cellular enzymatic assay) were assessed.RESULTSThere was more development of the glandular epithelium (P < 0.001) in SHR rats than in controls, which was even greater after doxazosin exposure (P = 0.027). SHR animals had higher caspase expression (P < 0.05) and activity (P = 0.008) than WKY rats, but both were reduced after doxazosin therapy (P < 0.01 and 0.028, respectively).CONCLUSIONSThis study confirmed prostate hyperplasia in the SHR model. Doxazosin exposure did not reduce the volume of glandular epithelium and contributed to protecting against caspase‐induced apoptosis. The SHR model may be not a valid option to study doxazosin‐induced apoptosis in BPH.

Purposes: To address prostate cancer (PCa) detection with respect to the number of biopsy sessions performed, to identify risk factors for detection after a negative biopsy, and to analyze the clinical characteristics of the detected tumors.Scope: Only biopsied men ( sextant) were included. A total of 1011 biopsy sessions were carried out in 770 men; 172 underwent a second prostate biopsy and 51 a third biopsy. During the first biopsy round, 111 cancers were found (14.4%), 27 in the second (15.7%), and five during the third round (9.8%), P = 0.156. Only high-grade PIN or atypia were identified as independent predictors or PCa detection in subsequent biopsies ( P = 0.008). A nonsignificant increase of clinically localized tumors, and a decrease of metastatic and poorly differentiated cases were found when more biopsy sessions were needed for detection.Conclusions: A nonsignificant trend to lower cancer detection rates and less clinical relevance of the tumors detected can be observed when more biopsy rounds are needed for detection.

Objective: To address detection rates and clinical features of the cancers detected with low prostate specific antigen (PSA) levels.Methods: In the context of a prostate cancer (PCa) screening program 1097 men attended to a new rescreen round. Sextant prostate biopsy was recommended when PSA greater than or equal to3 ng/ml. We also recommended to undergo biopsy in the range 1.0-2.99 ng/ml when free to total (f/t) PSA ratio less than or equal to20%. Detection rate was calculated and clinical features of the cancers detected were studied.Results: Mean age was 61.1 years. A total of 497 (45.3%) had total PSA <1.0 ng/ml, 439 (40%) between 1.0 and 2.99 ng/ml, and 161 (14.7%) &GE;3.0 ng/ml. In the group with PSA between 1.0 and 2.99 ng/ml and f/t PSA ratio &LE;20% a total of 249 biopsies were indicated (159 performed, acceptance 63.9%), and 15 cancers detected (detection rate 9.4%). Biopsy was recommended to 72 men with PSA between 3.0 and 3.99 ng/ml, performed in 56 (77.8%), and 12 tumors detected (detection rate 21.4%).All cancers in the study were clinically localized. Only 4 out of 15 cancers with PSA in the range 1.0-2.99 ng/ml (26.7%) fulfilled clinical criteria of insignificant cancer. Two were poorly differentiated and found to have patologically extracapsular disease. None of the 12 patients with PCa and PSA between 3.0 and 3.99 ng/ml had poorly differentiated features and only one complied with criteria of insignificant cancer. One out of seven who underwent RRP was found to have extracapsular disease.Conclusions: Cancer detection in low PSA ranges is lower but still relevant. The detection of potentially aggresive cancers is still of concern. (C) 2003 Elsevier B.V. All rights reserved.