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"tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "330" "paginaFinal" => "331" ] ] "autores" => array:1 [ 0 => array:3 [ "autoresLista" => "J. Rubio-Briones" "autores" => array:1 [ 0 => array:3 [ "nombre" => "J." "apellidos" => "Rubio-Briones" "email" => array:1 [ 0 => "jrubio@fivo.org" ] ] ] "afiliaciones" => array:1 [ 0 => array:1 [ "entidad" => "Servicio de Urología, Instituto Valenciano de Oncología, Valencia, Spain" ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "¿Qué podemos hacer para reconocer el cáncer de próstata de bajo riesgo?" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">At the request of the Editor of <span class="elsevierStyleItalic">Actas</span>, I am prepared in this Letter to the Editor to complement that of Dr. Vera,<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> and first I must admit that I adhere to his wise comments before what I consider the most important urological care problem in our specialty, overtreatment of low-risk prostate cancer (LR PCa).</p><p id="par0010" class="elsevierStylePara elsevierViewall">The aforementioned PIVOT study has confirmed what many urologists, I do not know if so many radiotherapists in own response to the letter from Dr. Vera, thought about LR PCa. However, I bear in mind that the slide that I have seen so many times in different conferences on the cat and tiger is not yet resolved. In the same U.S. Congress data that could be considered the same depth as the PIVOT have been presented; the ERSPC offers a reduction in the relative risk of metastatic progression of 31% at 12 years of follow-up, and with two more years of follow-up, decreased relative risk of death from PCa is observed in the screening group versus the control group of 0.40% (CI 95%: 0.17–0.64), requiring to treat only 12 men of those diagnosed to save one from dying from PCa,<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> data quite comparable to those from screening programs in breast cancer, currently covered by our health institutions. All this suggests to me that in the future the problem will be not in stopping diagnosing PCa, but in differentially managing the PCas detected in a screening that, covered or paid by the public health, will be performed in a more established way than at present. And within that differential management, I believe that active surveillance (AS) should play an important role.</p><p id="par0015" class="elsevierStylePara elsevierViewall">We cannot discredit before society the treatment of a tumor that, we must not forget, causes countless deaths a year in our country. Patients who had wanted an early diagnosis of their illness, and those for whom it would be a mistake to go against the evidence we have with screening. In my opinion, we must first imperiously look for molecular markers that allow us to recognize the tiger (as it is difficult for clinicopathologic markers to give more of themselves). We must test the new markers, which the same as PCA3 will complement, not replace, palpation and PSA, not only to save up to 49% of unnecessary biopsies,<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> but as prognostic factors that in isolation or combined with other molecular markers help us recognize which ‘low risk’ PCa we must actively treat and which can be included in active surveillance (AS). However, we have to keep in mind the hypothesis of late mutation of PCa, not early, to a more aggressive phenotype.</p><p id="par0020" class="elsevierStylePara elsevierViewall">Once the LR PCa is diagnosed, with a standardized biopsy of at least 10–12 cylinders, we must implement rigid criteria for inclusion in AS protocols, as also in the congress of the AUA an early repeat biopsy of 16 cylinders was shown, and the central review of these rejects at three months up to 41% of the patients initially candidates for AS with a 12-cylinder biopsy (A1095). The patient must understand a strategy in which they can progress in 14% of the cases at 4 years and in 25% of the cases at 6.8 years of follow-up,<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> and nevertheless be cured; they must also engage and be able to perform a close follow-up/compliance with evolutionary biopsies and must ultimately learn to live with the anxiety of not being treated. Reporting well should not be compared with convincing anyone.</p><p id="par0025" class="elsevierStylePara elsevierViewall">In this dilemma, I believe age is a decisive factor both to restrict biopsies and to implement AS. We know that PCa has a slow timeline, that observation of a cT1-2 PCa for over 15 years has a relative risk of 6.4 (2.3–17.8) of increase of that PCa mortality,<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> time probably higher in the PSA era due to the advancement that the use of this in the diagnosis of PCa (lead time bias) involves. On the other hand, our population ages with better and better quality of life indexes. Both realities must be seen when we inform a patient that he is a candidate for an AS protocol.</p><p id="par0030" class="elsevierStylePara elsevierViewall">Until we have better prognostic molecular panels, another reality to consider, and that in itself justifies our recommendation of a military protocol compliance of AS, is the 30% of the tumors that we have operated with LR PCa criteria and that the pathological anatomy shows that had been understaged and/or undergraded. The heterogeneity of PCa is treacherous. Currently, we include some patients in AS protocols and we are wrong; although most are redeemable with active treatment, in the event of progression, it is humane for the patient to think that they should not have performed AS and we have no arguments to say otherwise.</p><p id="par0035" class="elsevierStylePara elsevierViewall">Our goal as urologists is to continue increasing the decline in PCa mortality observed in European countries (from 15 to 12.5/100,000 men between 1995 and 2006, respectively).<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> To do this we will have to optimize the rational use of the weapons we have, such as the ERSPC risk calculator, and validate the new ones as they appear, delimiting all to their differential use according to age and prognostic panels. We will also have to validate new prognostic molecular markers for the patients already diagnosed. Finally, we will have to process all that information to patients with LR PCa for them to be the ones that choose the strategy to follow among the different alternatives, which hopefully in the future will be extended to focal therapy. And if they choose AS, we will have to agree when we have to actively treat without compromising the prognosis of our patient.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara">Please cite this article as: Rubio-Briones J. ¿Qué podemos hacer para reconocer el cáncer de próstata de bajo riesgo?. Actas Urol Esp. 2012;36:330–1.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:6 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "¿Estamos sobre tratando el cáncer de próstata de bajo riesgo?" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:1 [ 0 => "C.D. 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