1 CHUAC, A Coruña
2 CONTROVERSIAS EN EL SCREENING DEL CÁNCER DE PRÓSTATA: A QUIÉN Y CUÁNDO DEBO HACER UN PSA? Complexo Hospitalario Universitario de A Coruña
3 Introducción Discrimina el PSA Tumores y agresividad? CONTROVERSIAS EN EL SCREENING DEL CÁNCER DE PRÓSTATA: A QUIÉN Y CUÁNDO DEBO HACER UN PSA? Mejores Marcadores? Datos de despistaje? Pros y Cons del Despistaje? Cómo debemos estratificar Riesgos? Conclusiones
4 Center M. International variation in prostate cancer. Incidence and mortality rates. Eur Urol 2012; 61:
5 Jemal, Ca. Cancer J.Clin CA. PRÓSTATA - ESTADISTICAS R.P Sx bx PSA
7 Test de PSA? Riesgo Beneficio
8 Sensibilidad MARCADOR IDEAL Marcador Ideal SIMPLE DE OBTENER REPRODUCIBLE COSTE/EFECTIVO Especificidad
9 Introducción HBP & Cáncer de próstata El Dilema PSA
11 Progresión en el tiempo de las formas de PSA BPSA 10 30% Free PSA ppsa PSA Other ipsa* 70 90% PSA ACT Complex PSA PSA * ipsa= inactive PSA/not clipped/ not propsa ,5 4
12 PSA. Niveles Thompson IM, Pauler DK, Goodman PJ, Tangen CM, Lucia MS, Parnes HL, et al. Prevalence of prostate cancer among men with a prostate specific antigen level < or = 4.0 ng per milliliter. N Engl J Med. 2004; 350:
13 Relationship of total PSA, complexed PSA and % complexed PSA with the presence of tumor and tumor aggressiveness N=3098 biopsies Total PSA No Cancer (%) Cancer (%) Gleason <7 (%) Gleason 7 (%) Positive cores 2 (%) Relationship between total PSA, diagnosis of prostate cancer and tumor aggressiveness Positive cores >2 (%) TOTAL Gómez Veiga FG*, Ponce J, et al. Models to predict prostate cancer aggressiviness in patients candidates to biopsy with PSA J Urol 2011
14 Es esto suficiente? Qué factores influyen para que la biopsia pueda ser positiva, y si lo es que potencial de agresividad Puede tener? Edad, Volumen, PSA c, %C/T PSA, Tacto Rectal, Técnica de biopsia?
15 PSA y Detección PSA, ng/ml >10 DRE RESULTS BIOPSY % WITH CANCER BIOPSY % WITH CANCER BIOPSY % WITH CANCER BIOPSY % WITH CANCER Normal Indicative of cancer No Yes 1 5 No Yes Yes Yes Yes Yes >50 >75 Catalona WJ, et al. Use of the percentage of free prostate specific antigen to enhance differentiation of prostate cancer from bening prostatic disease. JAMA 1998; 279 (19):
16 Factores Efecto del volumen prostático y la DPSA y su relación con la agresividad PATIENT AND TUMOR CHARACTERISTICS IN RELATION TO PSA DENSITY PSAD (ng/ml/cc) < > 0.19 P Value Mean pt age ± SD 65 ± ± ± ± No. organ confined (%) 357 (82) 283 (75) 171 (75) 192 (55) <0.001 No. Gleason sum greater than 7 (%) 86 (20) 102 (27) 64 (28) 157 (45) <0.001 No. Tumor vol greater than 0.5 cc (%) 91 (21) 91 (25) 74 (33) 157 (56) <0.001 No. With progression (%) 26 (6) 31 (9) 22 (10) 67 (21) <0.001 Benson MC, et al. J Urol 1992; 147: PSA PSA En los pacientes con cáncer, la mayor agresividad histológica (Gleason >7) se corresponde con un volumen prostático menor que cuando el tumor es más indolente (33,5 ± 16,5 c.c. vs. 41,5 ± 21,6 c.c., p<0,001), relación que se también aplica si se considera la presencia o no de tejido tumoral en 2 o más cilindros de biopsia (40,3 ± 21,3 c.c. si 2 cilindros positivos, 34,9 ± 17,8c.c.si>2cilindros positivos, p<0,001).
17 PSA. Evolución. Velocidad 1 PSA. Cinética Detection of Life-Threatening Prostate Cancer With Prostate-Specifi c Antigen Velocity During a Window of CurabilityH. Ballentine Carter. J Natl Cancer Inst 2006;98: 1521 Men with PSA velocity above 0.35 ng/ml per year had a higher relative risk of prostate cancer death than men with PSA velocity of 0.35 ng/ml per year or less 0 2, PSA PSA. Evolución. Velocidad 2 0 2, PSA
18 PSA Edad? Comorbilidad?
19 Marcadores biológicos Calicreina humana 2 (hk2) Antígeno precoz de cáncer de próstaa (EPCA) Gen del cáncer de próstata 3 (PCA3) Genes de fusión TMPRSS2 ETS Factor de crecimiento β1(tgf β1) e interleucina 6 (IL6) Perfil proteómico microrna Glutation S transferasa (GSTP1) PSMA Marcadores Genéticos. SNP Cromogranin A (GRN A) 2 propsa
20 In contrast to the serum markers discussed previously, the new biomarker prostate cancer antigen 3 (PCA3) is measured in urine sediment obtained after prostatic massage. Determination of this PCa specific RNA is experimental. At a population level it appears to be helpful, but its impact at a single patient level remains highly questionable. Table 2 Guidelines for the diagnosis of prostate cancer Heidenreich A, et al. EAU Guidelines on prostate cancer. Part 1: screening, idagnosis, and treatment of clinically localised disease. Eur Urol, 2011;
22 Prostate cancer is the second most common cause of male cancer deaths in the United States. However, the full range of prostate cancer genomic alterations is incompletely characterized. Here we present the complete sequence of seven primary human prostate cancers and their paired normal counterparts. Several tumours contained complex chains of balanced (that is, copy neutral ) rearrangements that occurred within or adjacent to known cancer genes. Rearrangement breakpoints were enriched near open chromatin, androgen receptor and ERG DNA binding sites in the setting of the ETS gene fusion TMPRSS2 ERG, but inversely correlated with these regions in tumours lacking ETS fusions. This observation suggests a link between chromatin or transcriptional regulation and the genesis of genomic aberrations. Three tumours contained rearrangements that disrupted CADM2, and four harboured events disrupting either PTEN (unbalanced events), a prostate tumour suppressor, or MAGI2 (balanced events), a PTENinteracting protein not previously implicated in prostate tumorigenesis. Thus, genomic rearrangements may arise from transcriptional or chromatin aberrancies and engage prostate tumorigenic mechanisms. Science 2005; 310: Figure 4 Disruption of CADM2 and the PTEN pathway by rearrangements. a, Location of intragenic breakpoints in CADM2. b, CADM2 break apart demonstrated by FISH in an independent prostate tumour. c, Location of intragenic breakpoints in PTEN (top) and MAGI2 (bottom). d,magi2 inversion demonstrated by FISHin an independent prostate tumour, using probes flanking MAGI2 (red and green) and an external reference probe also on chromosome 7q (green). Berger MF, et al. The genomic complexity of primary human prostate cancer. Nature 2011; 470:
23 Genesis and Progression of Gene Fusions in Prostate Cancer Kumar Sinha C, et al. Recurrent gene fusions in prostate cancer. Nat Rev Cancer 2008; 8 (7):
24 Gamut of Gene Fusions in Prostate Cancer Kumar Sinha C, et al. Recurrent gene fusions in prostate cancer. Nat Rev Cancer 2008; 8 (7):
25 Bill-Axelson A, et al. Radical prostatectomy versus watchful waiting in early prostate cancer. N Engl J Med 2011; 364: Figure 2. Cumulative incidence of death from prostate cancer and development of metastases among men with lowrisk prostate cancer
26 Bill-Axelson A, et al. Radical prostatectomy versus watchful waiting in early prostate cancer. N Engl J Med. 2005; 352: Resultados a 5 y 10 años del seguimiento en pacientes con cáncer de próstata tratados con prostatectomía radical (PR) y esperar y ver (EV), en %
27 Bill-Axelson A, et al. Radical prostatectomy versus watchful waiting in early prostate cancer. N Engl J Med 2011; 364 (18): Figure 1. Cumulative Incidence of Death from Any Cause, Death from Prostate Cancer, and Development of Metastases. The cumulative incidence of death from any cause, death from prostate cancer, and development of metastases in the radical-prostatectomy group and the watchful-waiting group is shown in the total cohort (Panels A, B, and C), in men 65 years of age or older (Panels D, E, and F), and in men younger than 65 years of age (Panels G, H, and I).
29 Situación Schröder FH, et al. Prostate cancer mortality at 11 years of follow up. N Engl J Med. 2012; 366 (11): Schröder FH, et al. Screening and prostate cancer mortality in a randomized European study. N Engl J Med. 2009; 360:
30 Mortality results from the Göteborg randomised population-based prostate-cancer screening trial. Hugosson. Lancet Oncology 2011 Methods In December, 1994, men born between 1930 and 1944, randomly sampled from the population register, were randomised by computer in a 1:1 ratio to either a screening group invited for PSA testing every 2 years (n=10 000) or to a control group not invited (n=10 000). Men in the screening group were invited up to the upper age limit (median 69, range years) and only men with raised PSA concentrations were off ered additional tests such as digital rectal examination and prostate biopsies. The primary endpoint was prostate-cancer specifi c mortality, analysed according to the intention-to-screen principle. The study is ongoing, with men who have not reached the upper age limit invited for PSA testing. This is the fi rst planned report on cumulative prostate-cancer incidence and mortality calculated up to Dec 31, This study is registered as an International Standard Randomised Controlled Trial ISRCTN Findings In each group, 48 men were excluded from the analysis because of death or emigration before therandomisation date, or prevalent prostate cancer. In men randomised to screening, 7578 (76%) of 9952 attended atleast once. During a median follow-up of 14 years, 1138 men in the screening group and 718 in the control group were diagnosed with prostate cancer, resulting in a cumulative prostate-cancer incidence of 12 7% in the screening group and 8 2% in the control group (hazard ratio 1 64; 95% CI ; p<0 0001). The absolute cumulative risk reduction of death from prostate cancer at 14 years was 0 40% (95% CI ), from 0 90% in the control group to 0 50% in the screening group. The rate ratio for death from prostate cancer was 0 56 (95% CI ; p=0 002) in the screening compared with the control group. The rate ratio of death from prostate cancer for attendees compared with the control group was 0 44 (95% CI ; p=0 0002). Overall, 293 (95% CI ) men needed to be invited for screening and 12 to be diagnosed to prevent one prostate cancer death.
31 Mortality results from the Göteborg randomised population-based prostate-cancer screening trial. Hugosson. Lancet Oncology 2011
32 Between 1993 and 2001, of 76,693 men who were randomly assigned to usual care or intervention at 10 US centers, 73,378 (96%) completed a questionnaire that inquired about comorbidity and prostate specific antigen (PSA) testing before random assignment Fig 2. (A) Unadjusted cumulative incidence estimates14 of prostate cancer specific mortality in men with no or minimal comorbidity randomly assigned to usual care or intervention. k sample P.03. (B) Unadjusted cumulative incidence estimates14 of prostate cancer specific mortality in men with at least one significant comorbidity randomly assigned to usual care or intervention. k sample P=.07. Bonferroni adjustment16 for a significant P value was<.05 / 2 or.025 Crawford ED, et al. Comorbidity and mortality results from a randomized prostate cancer screening trial. J Clin Oncol, 2011; 29 (4):
33 Mejora Empeora Bouchardy C, et al. Recent trends in prostate cancer mortality show a continuous decrease in several countries. Int J Cancer 2008; 123:
34 Characteristics and methodological quality of randomised controlled trials of screening for prostate cancer No of participants randomised Study Screened group Control group Age range (years) Screening test Randomisatio n Allocation concealment Descripti on of loss to followup Blinding of outcome assessors Contamina tion (of control group) Intention to screen analysis Approximate median follow up time (years) Quebec PSA+DRE Adequate Not adeuate No Not adequate Not provided Not analysed but data provided 11 Norrkoping DRE initialy; PSA+DRE after 1993 Quasirandomi sation Not adequate Yes Not adequate Not provided Yes 13 (diagnosis) 15(death) ERSPC PSA+DRE Adquate Not adequate Unclear Yes Yes (20%) Yes 9 French ERSPC PSA Unclear Unclear Unclear Unclear Unclear Unclear 4 PLCO PSA+DRE Adequate Adequate Yes Yes Yes (40 52%) Yes 11.5 Gothenbur g PSA Adequate Not adequate Yes Yes Low, details not provided Yes 14 Djulbegovic M, et al. Screening for prostate cancer: systematic review and metaanalysis of randomised controlled trials. BMJ 2010; 341: c4543
35 Context Examining the tradeoffs between potential benefits and harms of prostate cancer screening is a hot topic. Contribution This updated systematic review for the U.S. Preventive Services Task Force found the following: screening based on prostate specific antigen led to detection of more cases of prostate cancer, small to no reduction in prostate cancer specific mortality after about 10 years, and several potential harms related to falsepositive test results and subsequent evaluations and therapies Caution Evidence regarding the mortality associated benefits of screening conflicted. Implication The clinical benefits of screening for prostate cancer remain uncertain. Consequences include evaluations and treatments that have associated complications and that may be unnecessary. Chou R, et al. Screening for Prostate Cancer: A Review of the Evidence for the U.S. Preventive Services Task Force. Ann Intern Med 2011; 155:
36 Summary of findings in trials on screening for prostate cancer Illustrative comparative risks (95% CI) Outcomes Event rate (per 1000) without screening Event rate (per 1000) with screening Relative risk (95% CI) No of participants Quality of evidence (GRADE) All cause mortality (inverse variance) Death from prostate cancer (inverse variance) Prostate cancer diagnosis (194 to 202) 0.99 (0.97 to 1.01) Moderate Moderate Low Effects of screening on stage: Stage I Stage II Stage III IV (13 to 34) 32 (23 to 45) 5 (4 to 5) 1.95 (1.22 to 3.13) 1.39 (0.99 to 1.95) 0.94 (0.85 to 1.04) Low Very low Moderate Djulbegovic M, et al. Screening for prostate cancer: systematic review and metaanalysis of randomised controlled trials. BMJ 2010; 341: c4543
37 Wilt TJ, et al. Radical prostatectomy versus observation for localized prostate cancer. N Engl J Med. 2012; 367 (3): PIVOT BACKGROUND The effectiveness of surgery versus observation for men with localized prostate cancer detected by means of prostate specific antigen (PSA) testing is not known. METHODS From November 1994 through January 2002, we randomly assigned 731 men with localized prostate cancer (mean age, 67 years; median PSA value, 7.8 ng per milliliter) to radical prostatectomy or observation and followed them through January The primary outcome was all cause mortality; the secondary outcome was prostatecancer mortality. Controversias Tratamiento el screening del cáncer del cáncer próstata de localizado próstata: y A localmente quién y cuándo avanzado debo hacer un PSA?
38 RESULTS Radical prostatectomy was associated with reduced all cause mortality among men with a PSA value greater than 10 ng per milliliter (P = 0.04 for interaction) and possibly among those with intermediate risk or high risk tumors (P = 0.07 for interaction). Adverse events within 30 days after surgery occurred in 21.4% of men, including one death. CONCLUSIONS Among men with localized prostate cancer detected during the early era of PSA testing, radical prostatectomy did not significantly reduce all cause or prostate cancer mortality, as compared with observation, through at least 12 years of follow up. Absolute differences were less than 3 percentage points. (Funded by the Department of Veterans Affairs Cooperative Studies Program and others; PIVOT ClinicalTrials.gov number, NCT ) Wilt TJ, et al. Radical prostatectomy versus observation for localized prostate cancer. N Engl J Med. 2012; 367 (3): Controversias Tratamiento el screening del cáncer del cáncer próstata de localizado próstata: y A localmente quién y cuándo avanzado debo hacer un PSA?
39 Figure 1. Study enrollment and treatment Wilt TJ, et al. Radical prostatectomy versus observation for localized prostate cancer. N Engl J Med. 2012; 367 (3): Controversias Tratamiento el screening del cáncer del cáncer próstata de localizado próstata: y A localmente quién y cuándo avanzado debo hacer un PSA?
40 Figure S2c-e. All-casue mortality by risk category: c: low risk; d: intermediate risk; e: hig risk Supplement to: Wilt TJ, Brawer MK, Jones KM, et al. Radical prostatectomy versus observation for localized prostate cancer. N Engl J Med 2012;367: OI: /NEJMoa Controversias Tratamiento el screening del cáncer del cáncer próstata de localizado próstata: y A localmente quién y cuándo avanzado debo hacer un PSA?
41 Flowchart of the comparison arm for ProtecT trial Lane JA, et al. Latest results from the UK trials evaluating prostate cancer screening and treatment: The CAP and ProtecT studies. Eur J Cancer 2010; 46:
42 . Design characteristics of the CAP trial and ERSPC TRIAL CHARACTERISTIC CAP TRIAL ERSPC Randomisation unit Location Eligibility criteria Recruitment period Recruitment total Intervention group: PSA threshold (total PSA) DRE with PSA testing Biopsy protocol Rescreening interval Treatment Control group Outcome ascertainment Primary outcome Follow up Quality of life Resource use Primary care centre United Kingdom Menaged50 60 years >550 (ca. 450,000 individuals) 3.0 ng/ml No 10 cores Not in protocol Localised disease: randomisation or choice of active monitoring, radiotherapy or surgery Advanced disease: local policy Usual clinical care Independent blinded adjudication committee Prostate cancer specific mortality Average 10 years (up to 2016) Across intervention group Across both groups Individual 7 European countries Menaged55 69 years ,243 individuals 3.0 ng/ml ( 4.0) Yes 6cores 4 years (2 7) Local policy Usual clinical care Independent blinded adjudication committee Prostate cancer specific mortality Median 9 years (up to 2007) Several centres Several centres Lane JA, et al. Latest results from the UK trials evaluating prostate cancer screening and treatment: The CAP and ProtecT studies. Eur J Cancer 2010; 46:
43 ESPECTATIVA DE VIDA EDAD ESPERANZA DE VIDA 37,11 32,08 27,70 23,48 19,50 15,71 12,21 9,16 6,65 4,75 3,36 2,61 Fuente: www. Ine.es acceso enero 2011
44 CLASIFICACIÓN Y VALORACIÓN DE RIESGO SEGÚN LAS COMORBILIDADES EN PACIENTES CANDIDATOS A CIRUGÍA. VALORACIÓN DEL RIESGO QUIRÚRGICO. Índice de Charlson Se considera: Ausencia de comorbilidad: 0-1 puntos Comorbilidad baja: 2 puntos Comorbilidad alta: > 3 puntos. Predicción de mortalidad/año a 3 años: Índice de 0: 12% Índice 1-2: 26% Índice 3-4: 52% Índice > 5: 85%
45 No se puede mostrar la imagen en este momento. DEFINIR POBLACIONES DE TUMORES Introducción Dr necesito hacer una biopsia?
47 MODELOS Análisis de los resultados aplicando los nomogramas Autor Referencia Año Nº ptes PSA rango (ng/ml) Bx/Nº cilindros 1ª bx/otras ABC Modelo Thompson J Natl Cancer Inst. 2006; 98, ,3-287? Múltiples 0,72 Regresión logística Nam J Clin Oncol. 2007; 25: , ? 0,74 cáncer 0,77 alto riesgo Regresión logística Kawakami Eur Urol. 2008; 54: <20 Media 22 0,75 cáncer 0,80 alto riesgo ANN Chun Eur Urol. 2007; 52: ? 0,8 Estudio J Urol , º 0,76 cáncer 0,82 alto riesgo 0,78 cilindros (+) Regresión logística Regresión logística
48 2147 pacientes PSA>3 Biopsia: sextante ABC: 0,77 Roobol MJ, et al. A Risk Based Strategy Improves Prostate Specific Antigen Driven Detection of Prostate Cancer. Eur Urol 2010, 79 85
50 Age-Adjusted Incidence Rates of Prostate Cancer Over Time and by Prescreen and Postcreen Snapshot Esseman L, et al. Rethinking screening for breast cancer and prostate cancer. JAMA. 2009; 302 (15):
51 After 20 years of screening for breast and prostate cancer, several observations can be made. First, the incidence of these cancers increased after the introduction of screening but has never returned to prescreening levels. Second, the increase in the relative fraction of early stage cancers has increased. Third, the incidence of regional cancers has not decreased at a commensurate rate. One possible explanation is that screening may be increasing the burden of low risk cancers without significantly reducing the burden of more aggressively growing cancers and therefore not resulting in the anticipated reduction in cancer mortality. To reduce morbidity and mortality from prostate cancer and breast cancer, new approaches for screening, early detection, and prevention for both diseases should be considered. Esseman L, et al. Rethinking screening for breast cancer and prostate cancer. JAMA. 2009; 302 (15):
52 Screen Detection Capability Based on Tumor Biology and Growth Rates Esseman L, et al. Rethinking screening for breast cancer and prostate cancer. JAMA. 2009; 302 (15):
53 Zeliadt SB, et al. Influence of Publication of US and European Prostate Cancer Screening Trials on PSA Testing Practices. J Natl Cancer Inst. 2011; 103(6):
54 Registro Nacional de cáncer de Próstata 2010 en España J M.Cozar, Miñana, G- Veiga. A Rodriguez et al. BJU int 2012 and Actas Españolas de Urologia 2012
55 Registro Nacional de cáncer de Próstata 2010 en España J M.Cozar, Miñana, G- Veiga. A Rodriguez et al. BJU int 2012 and Actas Españolas de Urologia 2012 Enfermedad Cardio-Vascular: 1968(48.15%)
56 Percentage of Voters in a Region in Favor of Prostate-Specific Antigen (PSA) Testing, According to Geographic Region. Colbert JA, et al. Prostate Cancer Screening Polling Results. N Engl J Med. 2012
57 Provisional Clinical Opinion On the basis of identified evidence and the expert opinion of the panel: In men with a life expectancy<10 years,* it is recommended that general screening for prostate cancer with total PSA be discouraged, because harms seem to outweigh potential benefits. Type and strength of recommendation. Evidence based: strong. Strength of evidence. Moderate:basedonfive randomizedclinicaltrials (RCTs) with intermediate to high risk of bias, moderate follow up, and limited data on subgroup populations. In men with a life expectancy>10 years,* it is recommended that physicians discuss with their patients whether PSA testing for prostate cancer screening is appropriate for them. PSA testing may save lives but is associated with harms, including complications, from unnecessary biopsy, surgery, or radiation treatment. Type and strength of recommendation. Evidence based: strong. Strength of evidence. For benefit, moderate; for harm, strong: based on five RCTs (and several cohort studies) with intermediate to high risk of bias, moderate follow up, indirect data, inconsistent results, and limited data on subgroup populations. It is recommended that information written in lay language be available to clinicians and their patients to facilitate the discussion of the benefits and harms associated with PSA testing before the routine ordering of a PSA test. Type and strength of recommendation. Informal consensus: strong. Strength of evidence. Indeterminate: evidence was not systematically reviewed to inform this recommendation; however, randomized trials are available on the topic. *Calculation of life expectancy is based on a variety of individual factors and circumstances. A number of life expectancy calculators (eg, are available in the public domain; however, ASCO does not endorse any one calculator over another. Basch E, et al. Screening for Prostate Cancer With Prostate-Specific Antigen Testing: American Society of Clinical Oncology Provisional Clinical Opinion. J Clin Oncol. 2012; 30 (24):
58 EUA (1) AUA (2) NCCN (3) Sociedad Americana Cancer (4) US TASK FORCE (5) Año Recomendación de Cribado sistemático No No No No Detección Precoz Edad Antecedentes Familiares Tacto rectal PSA (indicación biopsia) 2 3 2,5 4 2,5 4 2,5 4 Factores Riesgo PSA % PSAc/t <25 PSAv>0,75 ng/ml PSAv>0,75ng/ml Factores de Agresividad No No No No Técnica de biopsia Ecodirigida Ecodirigida Ecodirigida Ecodirigida Nº de punciones Edad límite >75 Expectativa <10 años Comorbilidades valoración Decisión de cribado y Biopsia >75* Expectativa <10 años Informada y compartida Informada y compartida Informada y compartida Informada y compartida
59 Case 1 PSA Biopsy: Gleason 7 (3+4), 9c+/10 90% + c. 47 year old man 1st PSA: 1.7ng/ml Rectal E.: Slightly fibrous Prostate volume: 22 cc Weight: 72kg Height: 1.72m. No Comorbidities Family history of PC
60 CONCLUSIONES El PSA reduce muertes por cáncer de próstata. El nivel inicial de PSA debe ser inferior a 4, 2,5-3 en pacientes con expectativa de vida mayor de 10 años. Las características del paciente son fundamentales para indicar test. La edad en la que recomendar no hacer determinación no está definida pero en varones mayores de 75 no parece ser beneficioso. Los modelos nos pueden ayudar a tomar la decisión con el paciente Nuevos marcadores están en marcha, pero no sustituyen al PSA en la actualidad. Importante informar y consensuar con el paciente riesgos-beneficios, Screening.no, despistaje sí...