Draft Recommendation Statement
Screening for Prostate Cancer: U.S. Preventive Services Task Force Recommendation Statement
Summary of Recommendation and Evidence
Benefits of Detection and Early Intervention
Harms of Detection and Early Intervention
Patient Population Under Consideration
Research Needs and Gaps
Burden of Disease
Scope of Review
Accuracy of Screening
Effectiveness of Early Detection and Treatment
Harms of Screening and Treatment
Estimate of Magnitude of Net Benefit
How Does Evidence Fit With Biological Understanding?
Update of Previous USPSTF Recommendation
Recommendations of Others
Appendix: U.S. Preventive Services Task Force
Table 1: What the Grades Mean and Suggestions for Practice
Table 2: Levels of Certainty Regarding Net Benefit
|Level of Certainty||Description|
|High||The available evidence usually includes consistent results from well-designed, well-conducted studies in representative primary care populations. These studies assess the effects of the preventive service on health outcomes. This conclusion is therefore unlikely to be strongly affected by the results of future studies.|
|Moderate||The available evidence is sufficient to determine the effects of the preventive service on health outcomes, but confidence in the estimate is constrained by factors such as:
As more information becomes available, the magnitude or direction of the observed effect could change, and this change may be large enough to alter the conclusion.
|Low||The available evidence is insufficient to assess effects on health outcomes. Evidence is insufficient because of:
More information may allow an estimation of effects on health outcomes.
2. Thompson IM, Goodman PJ, Tangen CM, Lucia MS, Miller GJ, et al. The influence of finasteride on the development of prostate cancer. N Engl J Med. 2003;349:215-24.
3. Wilt TJ. The VA/NCI/AHRQ Cooperative Studies Program #407: Prostate cancer Intervention Versus Observation Trial (PIVOT): main results from a randomized trial comparing radical prostatectomy to watchful waiting in men with clinically localized prostate cancer. Paper presented at: 107th Annual Meeting of the American Urological Association; May 2011; Washington, DC.
4. Schröder FH, Hugosson J, Roobol MJ, Tammela TL, Ciatto S, et al. Screening and prostate-cancer mortality in a randomized European study. N Engl J Med. 2009;360:1320-8.
5. Lin K, Lipsitz R, Miller T, Janakiraman S; U.S. Preventive Services Task Force. Benefits and harms of prostate-specific antigen screening for prostate cancer: an evidence update for the U.S. Preventive Services Task Force. Ann Intern Med. 2008;149:192-9.
6. Chou R, Croswell JM, Dana T, Bougatsos C, Blazina I, et al. Screening for prostate cancer: a review of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med. 2011 Oct 7. [Epub ahead of print]
7. Lin K, Croswell JM, Koenig H, Lam C, Maltz A. Prostate-Specific Antigen-Based Screening for Prostate Cancer: An Evidence Update for the U.S. Preventive Services Task Force. Evidence Synthesis No. 90. AHRQ Publication No. 12-05160-EF-1. Rockville, MD: Agency for Healthcare Research and Quality; 2011.
8. Chou R, Dana T, Bougatsos C, Fu R, Blazina I, et al. Treatments for Localized Prostate Cancer: Systematic Review to Update the 2002 U.S. Preventive Services Task Force Recommendation. Evidence Synthesis No. 91. AHRQ Publication No. 12-05161-EF-2. Rockville, MD: Agency for Healthcare Research and Quality; 2011.
9. Bill-Axelson A, Holmberg L, Ruutu M, Garmo H, Stark JR, et al. Radical prostatectomy versus watchful waiting in early prostate cancer. N Engl J Med. 2011;364:1708-17.
10. Ilic D, O’Connor D, Green S, Wilt TJ. Screening for prostate cancer: an updated Cochrane systematic review. BJU Int. 2011;107:882-91.
11. Andriole GL, Crawford ED, Grubb RL 3rd, Buys SS, Chia D, et al. Mortality results from a randomized prostate-cancer screening trial. N Engl J Med. 2009;360:1310-9.
12. Labrie F, Candas B, Cusan L, Gomez JL, Bélanger A, et al. Screening decreases prostate cancer mortality: 11-year follow-up of the 1988 Quebec prospective randomized controlled trial. Prostate. 2004;59:311-8.
13. Sandblom G, Varenhorst E, Rosell J, Löfman O, Carlsson P. Randomised prostate cancer screening trial: 20 year follow-up. BMJ. 2011;342:d1539.
14. Kjellman A, Akre O, Norming U, Törnblom M, Gustafsson O. 15-year followup of a population based prostate cancer screening study. J Urol. 2009;181:1615-21.
15. Djulbegovic M, Beyth RJ, Neuberger MM, Stoffs TL, Vieweg J, et al. Screening for prostate cancer: systematic review and meta-analysis of randomised controlled trials. BMJ. 2010;341:c4543.
16. Hugosson J, Carlsson S, Aus G, Bergdahl S, Khatami A, et al. Mortality results from the Göteborg randomised population-based prostate-cancer screening trial. Lancet Oncol. 2010;11:725-32.
17. Wilt TJ, MacDonald R, Rutks I, Shamliyan TA, Taylor BC, Kane RL. Systematic review: comparative effectiveness and harms of treatments for clinically localized prostate cancer.Ann Intern Med. 2008;148:435-48.
18. Welch HG, Albertsen PC. Prostate cancer diagnosis and treatment after the introduction of prostate-specific antigen screening: 1986–2005. J Natl Cancer Inst. 2009;101:1325-9.
19. Wilt TJ, Brawer MK, Barry MJ, Jones KM, Kwon Y, et al. The Prostate cancer Intervention Versus Observation Trial: VA/NCI/AHRQ Cooperative Studies Program #407 (PIVOT): design and baseline results of a randomized controlled trial comparing radical prostatectomy to watchful waiting for men with clinically localized prostate cancer. Contemp Clin Trials. 2009;30:81-7.
20. Moore AL, Dimitropoulou P, Lane A, Powell PH, Greenberg DC, et al. Population-based prostate-specific antigen testing in the UK leads to a stage migration of prostate cancer.BJU Int. 2009;104:1592-8.
21. Theoret MR, Ning YM, Zhang JJ, Justice R, Keegan P, Pazdur R. The risks and benefits of 5a-reductase inhibitors for prostate-cancer prevention. N Engl J Med. 2011;365:97-9.
22. American Cancer Society. Cancer Facts & Figures 2010. Atlanta: American Cancer Society; 2010. Accessed athttp://www.cancer.org/Research/CancerFactsFigures/CancerFactsFigures/cancer-facts-and-figures-2010 on 6 October 2011.
23. Sakr WA, Haas GP, Cassin BF, Pontes JE, Crissman JD. The frequency of carcinoma and intraepithelial neoplasia of the prostate in young male patients. J Urol. 1993;150:379-85.
24. Grönberg H. Prostate cancer epidemiology. Lancet. 2003;361:859-64.
25. U.S. Preventive Services Task Force. Screening for prostate cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2008;149:185-91.
26. Welch HG, Schwartz LM, Woloshin S. Prostate-specific antigen levels in the United States: implications of various definitions for abnormal. J Natl Cancer Inst. 2005;97:1132-7.
27. Thompson IM, Ankerst DP, Chi C, Lucia MS, Goodman PJ, et al. Operating characteristics of prostate-specific antigen in men with an initial PSA level of 3.0 ng/ml or lower. JAMA. 2005;294:66-70.
28. Vickers AJ, Till C, Tangen CM, Lilja H, Thompson IM. An empirical evaluation of guidelines on prostate-specific antigen velocity in prostate cancer detection. J Natl Cancer Inst. 2011;103:462-9.
29. Wolters T, Roobol MJ, Steyerberg EW, van den Bergh RC, Bangma CH, et al. The effect of study arm on prostate cancer treatment in the large screening trial ERSPC. Int J Cancer. 2010;126:2387-93.
30. Bill-Axelson A, Holmberg L, Filén F, Ruutu M, Garmo H, et al. Radical prostatectomy versus watchful waiting in localized prostate cancer: the Scandinavian Prostate Cancer Group-4 randomized trial. J Natl Cancer Inst. 2008;100:1144-54.
31. Croswell JM, Kramer BS, Kreimer AR, Prorok PC, Xu JL, et al. Cumulative incidence of false-positive results in repeated, multimodal cancer screening. Ann Fam Med. 2009;7:212-22.
32. McNaughton-Collins M, Fowler FJ Jr, Caubet JF, Bates DW, Lee JM, et al. Psychological effects of a suspicious prostate cancer screening test followed by a benign biopsy result. Am J Med. 2004;117:719-25.
33. Fowler FJ Jr, Barry MJ, Walker-Corkery B, Caubet JF, Bates DW, et al. The impact of a suspicious prostate biopsy on patients’ psychological, socio-behavioral, and medical care outcomes. J Gen Intern Med. 2006;21:715-21.
34. Raaijmakers R, Kirkels WJ, Roobol MJ, Wildhagen MF, Schröder FH. Complication rates and risk factors of 5802 transrectal ultrasound-guided sextant biopsies of the prostate within a population-based screening program. Urology. 2002;60:826-30.
35. De Sio M, D’Armiento M, Di Lorenzo G, Damiano R, Perdonà S, et al. The need to reduce patient discomfort during transrectal ultrasonography-guided prostate biopsy: what do we know? BJU Int. 2005;96:977-83.
36. Welch HG, Black WC. Overdiagnosis in cancer. J Natl Cancer Inst. 2010;102:605-13.
37. Draisma G, Boer R, Otto SJ, van der Cruijsen IW, Damhuis RA, et al. Lead times and overdetection due to prostate-specific antigen screening: estimates from the European Randomized Study of Screening for Prostate Cancer. J Natl Cancer Inst. 2003;95:868-78.
38. Hu JC, Gu X, Lipsitz SR, Barry MJ, D’Amico AV, et al. Comparative effectiveness of minimally invasive vs open radical prostatectomy. JAMA. 2009;302:1557-64.
39. Lu-Yao GL, Albertsen PC, Moore DF, Shih W, Lin Y, et al. Survival following primary androgen deprivation therapy among men with localized prostate cancer. JAMA. 2008;300:173-81.
40. Lu-Yao G, Stukel TA, Yao SL. Changing patterns in competing causes of death in men with prostate cancer: a population based study. J Urol. 2004;171:2285-90.
41. Albertsen PC, Hanley JA, Fine J. 20-year outcomes following conservative management of clinically localized prostate cancer. JAMA. 2005;293: .
42. Lu-Yao GL, Albertsen PC, Moore DF, Shih W, Lin Y, et al. Outcomes of localized prostate cancer following conservative management. JAMA. 2009;302:1202-9.
43. Carroll P, Albertsen PC, Greene K, Babaian RJ, Carter HB, et al. Prostate-Specific Antigen Best Practice Statement: 2009 Update. Linthicum, MD: American Urological Assocation; 2009. Accessed at http://www.auanet.org/content/guidelines-and-quality-care/clinical-guidelines/main-reports/psa09.pdf on 6 October 2011.
44. Wolf AM, Wender RC, Etzioni RB, Thompson IM, D’Amico AV, et al. American Cancer Society guideline for the early detection of prostate cancer: update 2010. CA Cancer J Clin. 2010;60:70-98.
45. American College of Physicians. Screening for prostate cancer. Ann Intern Med. 1997;126:480-4.
46. Lim LS, Sherin K; ACPM Prevention Practice Committee. Screening for prostate cancer in U.S. men: ACPM Position Statement on Preventive Practice. Am J Prev Med. 2008;34:164-70.
The draft recommendation, by the United States Preventive Services Task Force and due for official release next week, is based on the results of five well-controlled clinical trials and could substantially change the care given to men 50 and older. There are 44 million such men in the United States, and 33 million of them have already had a P.S.A. test — sometimes without their knowledge — during routine physicals.
Editorial del NEJM 26 de Marzo 2009
In the United States, most men over the age of 50 years have had a prostate-specific–antigen (PSA) test,1 despite the absence of evidence from large, randomized trials of a net benefit. Moreover, about 95% of male urologists and 78% of primary care physicians who are 50 years of age or older report that they have had a PSA test themselves,2 a finding that suggests they are practicing what they preach. And indeed, U.S. death rates from prostate cancer have fallen about 4% per year since 1992, five years after the introduction of PSA testing.3 Perhaps the answer to the PSA controversy is already staring us in the face. At the same time, practice guidelines cite the unproven benefit of PSA screening, as well as the known side effects,4,5 which largely reflect the high risks of overdiagnosis and overtreatment that PSA-based screening engenders.6
The first reports from two large, randomized trials that many observers hoped would settle the controversy appear in this issue of the Journal. In the U.S. Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, Andriole et al.7 report no mortality benefit from combined screening with PSA testing and digital rectal examination during a median follow-up of 11 years.8 In the European Randomized Study of Screening for Prostate Cancer (ERSPC) trial, Schröder et al.8 report that PSA screening without digital rectal examination was associated with a 20% relative reduction in the death rate from prostate cancer at a median follow-up of 9 years, with an absolute reduction of about 7 prostate cancer deaths per 10,000 men screened.8 The designs of the two trials are different and provide complementary insights.
First, one must ask, “Why were these results published now?” Neither set of findings seems definitive; that is, there was neither a clear declaration of futility in the PLCO trial nor an unambiguous net benefit in the ERSPC trial. Both studies are ongoing, with future updates promised. The report on the ERSPC trial follows a third planned interim analysis, which found a marginally significant decrease in prostate-cancer mortality after adjustment of the P value for the two previous looks in an attempt to avoid a false positive conclusion (yet apparently preserving no alpha for the planned final analysis). On the other hand, the investigators in the PLCO trial made the decision to publish their results now because of concern about the emerging evidence of net harm compared with potential benefits associated with PSA screening. Both decisions to publish now can be criticized as premature, leaving clinicians and patients to deal with the ambiguity.
The ERSPC trial is actually a collection of trials in different countries with different eligibility criteria, randomization schemes, and strategies for screening and follow-up. The report by Schröder et al. is based on a predefined core group of men between 55 and 69 years of age at study entry. Subjects were generally screened every 4 years, and 82% were screened at least once. Contamination of the control group with screening as part of usual care is not described. Biopsies were generally recommended for subjects with PSA levels of more than 3.0 ng per milliliter. It is unclear whether the clinicians and hospitals treating patients with prostate cancer differed between the two study groups.
Adjudications of causes of death were made by committees whose members were unaware of study-group assignments, though not of treatments. This point is important, since previous research has suggested that the cause of death is less likely to be attributed to prostate cancer among men receiving attempted curative treatment.9 Misattribution might then create a bias toward screening, since the diagnosis of more early-stage cancers in the ERSPC trial led to substantially more attempted curative treatments.
The ERSPC interim analysis revealed a 20% reduction in prostate-cancer mortality; the adjusted P value was 0.04. The estimated absolute reduction in prostate-cancer mortality of about 7 deaths per 10,000 men after 9 years of follow-up, if real and not the result of chance or bias, must be weighed against the additional interventions and burdens. The 73,000 men in the screening group underwent more than 17,000 biopsies, undoubtedly many more than did men in the control group, though the latter is not reported. Men had a substantially higher cumulative risk of receiving the diagnosis of prostate cancer in the screening group than in the control group (820 vs. 480 per 10,000 men). Diagnosis led to more treatment, with 277 versus 100 per 10,000 men undergoing radical prostatectomy and 220 versus 123 per 10,000 undergoing radiation therapy with or without hormones, respectively (tentative estimates given the unknown treatments in both groups).
Although estimates of the benefit of screening were somewhat greater for men who actually underwent testing (taking into account noncompliance) than for those who were not tested, the side effects would be proportionately higher as well. Given these trade-offs, the promise of future ERSPC analyses addressing quality of life and cost-effectiveness is welcome indeed. The ERSPC results also reemphasize the need for caution in screening men over the age of 69 years, given an early trend toward higher prostate-cancer mortality with screening in this age subgroup, although this finding may well be due to chance alone.
A final point to make about the ERSPC trial is that to the extent that the diagnosis and treatment of prostate cancer in the screening group differed from those in the control group, it becomes difficult to dissect out the benefit attributable to screening versus improved treatment once prostate cancer was suspected or diagnosed. A similar distribution of treatments among seemingly similar patients with cancer is only partially reassuring in this regard.
Despite a longer median follow-up, the PLCO trial was smaller and therefore less mature than the ERSPC trial, with 174 prostate-cancer deaths driving the power of the study, as compared with 540 such deaths in the ERSPC trial. The screening protocol was homogeneous across sites with an enrollment age of 55 to 74 years and annual PSA tests for 6 years and digital rectal examinations for 4 years, with about 85% compliance. Subjects in the screening group who had a suspicious digital rectal examination or a PSA level of more than 4.0 ng per milliliter received a recommendation for further evaluation. This strategy helped to ensure that any difference in outcome was attributable to screening, rather than downstream management. The effectiveness of screening, of course, will be determined by the effectiveness of subsequent “usual care,” but this is the same usual care that many practitioners assume has been responsible for the falling U.S. death rate from prostate cancer. Adjudication of causes of death was similar to that in the ERSPC trial.
Though the PLCO trial has shown no significant effect on prostate-cancer mortality to date, the relatively low number of end points begets a wide confidence interval, which includes at its lower margin the point estimate of effect from the ERSPC trial. Other likely explanations for the negative findings are high levels of prescreening in the PLCO population and contamination of the control group. Contamination was assessed by periodic cross-sectional surveys, with about half the subjects in the control group undergoing PSA testing by year 5. It is unclear whether these estimates reflect testing that year or since trial inception; if the former, the cumulative incidence may be even higher. The smaller difference in screening intensity between the two study groups in the PLCO trial, as compared with the ERSPC trial, is reflected in a smaller risk of overdiagnosis (23% vs. more than 70%) and a less impressive shift in cancer stage and grade distributions. Given that study-group contamination from the use of digital rectal examination was less problematic (only about 25%), ongoing results from both of these trials may necessitate rethinking the role of digital rectal examination in cancer screening.
After digesting these reports, where do we stand regarding the PSA controversy? Serial PSA screening has at best a modest effect on prostate-cancer mortality during the first decade of follow-up. This benefit comes at the cost of substantial overdiagnosis and overtreatment. It is important to remember that the key question is not whether PSA screening is effective but whether it does more good than harm. For this reason, comparisons of the ERSPC estimates of the effectiveness of PSA screening with, for example, the similarly modest effectiveness of breast-cancer screening cannot be made without simultaneously appreciating the much higher risks of overdiagnosis and overtreatment associated with PSA screening.
The report on the ERSPC trial appropriately notes that 1410 men would need to be offered screening and an additional 48 would need to be treated to prevent one prostate-cancer death during a 10-year period, assuming the point estimate is correct. And although the PLCO trial may not have the power as yet to detect a similarly modest benefit of screening, its power is already more than adequate to detect important harm through overdiagnosis. However, the implications of the trade-offs reflected in these data, like beauty, will be in the eye of the beholder. Some well-informed clinicians and patients will still see these trade-offs as favorable; others will see them as unfavorable. As a result, a shared decision-making approach to PSA screening, as recommended by most guidelines, seems more appropriate than ever.
Finally, despite these critiques, both groups of investigators deserve high praise for their persistence and perseverance: to manage such monstrous trials is a herculean task, made no easier when so many observers think the results are self-evident. Further analyses will be needed from these trials, as well as from others — such as the Prostate Cancer Intervention Versus Observation Trial (PIVOT) in the United States (ClinicalTrials.gov number, NCT00007644 [ClinicalTrials.gov] )10 and the Prostate Testing for Cancer and Treatment (PROTECT) trial in the United Kingdom (Current Controlled Trials number, ISRCTN20141297 [controlled-trials.com] )11 — if the PSA controversy is finally to sleep the big sleep.
No potential conflict of interest relevant to this article was reported.
From Massachusetts General Hospital and Harvard Medical School, Boston.
This article (10.1056/NEJMe0901166) was published at NEJM.org on March 18, 2009.
- Ross LE, Berkowitz Z, Ekwueme DU. Use of the prostate-specific antigen test among U.S. men: findings from the 2005 National Health Interview Survey. Cancer Epidemiol Biomarkers Prev 2008;17:636-644. [Free Full Text]
- Chan EC, Barry MJ, Vernon SW, Ahn C. Brief report: physicians and their personal prostate cancer-screening practices with prostate-specific antigen: a national survey. J Gen Intern Med 2006;21:257-259. [CrossRef][ISI][Medline]
- Ries LAG, Melbert D, Krapcho M, et al. SEER cancer statistics review, 1975–2005. Bethesda, MD: National Cancer Institute, 2008. (Accessed March 6, 2009 at http://seer.cancer.gov/csr/1975_2005/.)
- Smith RA, Cokkinides V, Brawley OW. Cancer screening in the United States, 2008: a review of current American Cancer Society guidelines and cancer screening issues. CA Cancer J Clin 2008;58:161-179. [Free Full Text]
- U. S. Preventive Services Task Force. Screening for prostate cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2008;149:185-191. [Free Full Text]
- Barry MJ. Why are a high overdiagnosis probability and a long lead time for prostate cancer screening so important? J Natl Cancer Inst (in press).
- Andriole GL, Grubb RL III, Buys SS, et al. Mortality results from a randomized prostate-cancer screening trial. N Engl J Med 2009;360:1310-1319. [Free Full Text]
- Schröder FH, Hugosson J, Roobol MJ, et al. Screening and prostate-cancer mortality in a randomized European study. N Engl J Med 2009;360:1320-1328. [Free Full Text]
- Newschaffer CJ, Otani K, McDonald MK, Penberthy LT. Causes of death in elderly prostate cancer patients and in a comparison nonprostate cancer cohort. J Natl Cancer Inst 2000;92:613-621. [Free Full Text]
- Wilt TJ, Brawer MK, Barry MJ, et al. The Prostate cancer Intervention Versus Observation Trial: VA/NCI/AHRQ Cooperative Studies Program #407 (PIVOT): design and baseline results of a randomized controlled trial comparing radical prostatectomy to watchful waiting for men with clinically localized prostate cancer. Contemp Clin Trials 2009;30:81-87. [CrossRef][ISI][Medline]
- Donovan J, Hamdy F, Neal D, et al. Prostate Testing for Cancer and Treatment (ProtecT) feasibility study. Health Technol Assess 2003;7:1-88. [Medline]
La prueba, dicen los investigadores de la Universidad de Michigan, puede ayudar a un individuo a decidir si debe someterse a una biopsia.
El análisis detecta un defecto genético, que según los científicos, muestra la presencia de la enfermedad en la mitad de los tumores de próstata.
Niveles de PSA
Actualmente para detectar los primeros signos de la enfermedad se miden los niveles del antígeno prostático específico o PSA en la sangre.
Sin embargo, estos análisis han sido controvertidos porque los niveles elevados de PSA no necesariamente significan la presencia de cáncer lo cual puede conducir a diagnósticos equivocados.
Un PSA elevado en la sangre puede mostrar la presencia de cáncer, pero también puede ser un indicio de otros trastornos, como un ensanchamiento de la próstata o una infección urinaria.
De la misma forma, una prueba normal de PSA no garantiza que un hombre no tenga un tumor, lo cual significa una oportunidad perdida para tratamiento temprano.
“Pensamos que va a ser una herramienta que ayudará a los hombres con PSA elevado a decidir si necesitan una biopsia o si pueden retrasar el procedimiento“
Como el cáncer de próstata se ha convertido en el cáncer más común en los hombres y la segunda causa de muerte por cáncer en muchos países del mundo, existe una necesidad urgente de crear métodos diagnósticos más precisos.
Y desde hace tiempo varios equipos de investigadores en el mundo trabajan en el desarrollo de una prueba de orina.
La nueva prueba, creada por científicos de la Universidad de Michigan, identifica una anormalidad genética que ocurre en cerca de la mitad de todos los tumores de próstata.
En ésta dos genes cambian de lugar y se fusionan causando una mutación que, según los científicos, causa el cáncer.
Tal como señalan los investigadores en Science Translational Medicine (Science, Medicina Traslacional), los estudios llevados a cabo muestran que la fusión genética, llamada TMPRSS:ERG, “casi siempre indica la presencia de cáncer”.
Pero como este defecto sólo está presente en la mitad de los tumores prostáticos, los científicos también incluyeron en el análisis otro marcador, llamado PCA3, lo cual hace que el análisis sea más preciso.
Los científicos esperan que la prueba sea un complemento del análisis de PSA, y con ambos resultados se pueda tomar una decisión mejor informada sobre el siguiente paso, por ejemplo, si hay necesidad de someterse a una biopsia o no.
Las biopsias son pruebas invasivas e incómodas en las que es necesario introducir una aguja para extraer una muestra de tejido.
Y tampoco ofrecen un panorama completo de la glándula porque es una prueba de una muestra pequeña de la próstata, de manera que también puede dar resultados falsos.
Los científicos llevaron a cabo pruebas de orina con 1.300 pacientes en tres centros médicos académicos y siete hospitales del país.
Todos habían mostrado niveles elevados de PSA y habían acudido a las clínicas para someterse a una biopsia o a una prostatectomía, una cirugía para extraer parte o toda la próstata.
Los investigadores llevaron a cabo el análisis en muestras de orina de los pacientes y los dividieron en grupos de bajo, intermedio y alto riesgo de cáncer.
Posteriormente compararon esos resultados con los de las biopsias.
Encontraron que las biopsias mostraron cáncer en 21% de los pacientes del grupo de bajo riesgo, 43% de los de riesgo intermedio y 69% del grupo de alto riesgo.
La prueba de orina, sin embargo, mostró que sólo 7% de los hombres del grupo de bajo riesgo y 40% del grupo de alto riesgo tenían un tumor agresivo.
Por otra parte las pruebas de PSA mostraron que muchos hombres con PSA elevado no tenían cáncer.
Tal como señala el doctor Scott Tomlins, quien dirigió el estudio, “aquí es donde esta prueba realmente puede ayudar”.
“El análisis del TMPRSS2:ERG y PCA3 mejora significativamente la capacidad de predecir si un hombre tiene cáncer de próstata” afirma.
“Pensamos que va a ser una herramienta que ayudará a los hombres con PSA elevado a decidir si necesitan una biopsia o si pueden retrasar el procedimiento”, agrega.
Los científicos esperan que el análisis esté listo para uso en la clínica en Estados Unidos dentro de un año.