Corresponding author at: University Hospitals Case Medical Center, 11100 Euclid Avenue, Cleveland, OH 44106, United States.
que se leu este artigo
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"en" => array:12 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Original article</span>" "titulo" => "Tumor suppressor p53 protein expression: prognostic significance in patients with low-risk myelodysplastic syndrome" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "196" "paginaFinal" => "201" ] ] "contieneResumen" => array:1 [ "en" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0015" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 798 "Ancho" => 1535 "Tamanyo" => 73016 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Event-free survival curve of patients with low risk myelodysplastic syndrome and positive or negative for p53.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Fernando Barroso Duarte, Romelia Pinheiro Gonçalves, Maritza Cavalcante Barbosa, Francisco Dário Rocha Filho, Talyta Ellen de Jesus dos Santos, Thayna Nogueira dos Santos, Paulo Roberto Leitão de Vasconcelos" "autores" => array:7 [ 0 => array:2 [ "nombre" => "Fernando Barroso" "apellidos" => "Duarte" ] 1 => array:2 [ "nombre" => "Romelia Pinheiro" "apellidos" => "Gonçalves" ] 2 => array:2 [ "nombre" => "Maritza Cavalcante" "apellidos" => "Barbosa" ] 3 => array:2 [ "nombre" => "Francisco Dário" "apellidos" => "Rocha Filho" ] 4 => array:2 [ "nombre" => "Talyta Ellen" "apellidos" => "de Jesus dos Santos" ] 5 => array:2 [ "nombre" => "Thayna Nogueira" "apellidos" => "dos Santos" ] 6 => array:2 [ "nombre" => "Paulo Roberto Leitão" "apellidos" => "de Vasconcelos" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S1516848414000085?idApp=UINPBA00005G" "url" => "/15168484/0000003600000003/v3_201411060108/S1516848414000085/v3_201411060108/en/main.assets" ] ] "en" => array:11 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Scientific Comment</span>" "titulo" => "Utility of the p53 mutant protein in patients with low-risk myelodysplastic syndrome" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "173" "paginaFinal" => "174" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "David C. Yao, Marcos de Lima" "autores" => array:2 [ 0 => array:3 [ "nombre" => "David C." "apellidos" => "Yao" "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 1 => array:4 [ "nombre" => "Marcos" "apellidos" => "de Lima" "email" => array:1 [ 0 => "Marcos.deLima@uhhospitals.org" ] "referencia" => array:3 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] 2 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "University Hospitals Case Medical Center, Cleveland, United States" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Seidman Cancer Center and Case Western Reserve University, Cleveland, United States" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "<span class="elsevierStyleItalic">Corresponding author at</span>: University Hospitals Case Medical Center, 11100 Euclid Avenue, Cleveland, OH 44106, United States." ] ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">In this issue of the Revista Brasileira de Hematologia e Hemoterapia, Duarte et al.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> present data on the role of p53 protein expression and prognosis of patients with low-risk myelodysplastic syndrome (MDS). In a cohort of 38 patients, the authors demonstrated an association between mutant p53 protein expression and shortened survival.</p><p id="par0010" class="elsevierStylePara elsevierViewall">MDS is a clinically heterogeneous disorder.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Patients with this condition demonstrate clonal hematopoietic expansion, cytopenias, myelodysplasia, ineffective hematopoiesis and an increased propensity to develop acute myeloid leukemia. Not surprisingly, prognosis is related to severity of cytopenias, presence of cytogenetic abnormalities and clonal evolution demonstrated by blast counts, and other ‘traditional’ prognostic elements. There is heterogeneity even among patients diagnosed with lower-risk disease, since a subset of these patients have more aggressive disease. Recent efforts have demonstrated that several molecular parameters linked to the pathophysiology of MDS may affect overall survival.<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3,4</span></a> Thus, identification of additional prognosticators that more accurately characterize subgroups and their outcomes are essential.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Current understanding of the pathophysiology of MDS indicates that there are founding mutations in a hematopoietic stem cell that ultimately offer a survival advantage to the affected cell(s). These mutations occur in genes encoding protein products that are involved typically in either RNA splicing or DNA methylation, which in turn leads to genomic instability and further mutations.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> The survival advantage in mutated cells usually leads to a dominant bone marrow progenitor clone. This clone can subsequently acquire additional driver mutations that lead to the development of multiple subclonal populations. The accumulation and combination of these genetic lesions likely contribute to the phenotypes observed in MDS patients. <span class="elsevierStyleItalic">TP53</span> gene mutations are particularly interesting given the fact that its protein product has tumor suppression activity.</p><p id="par0020" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">TP53</span> encodes a cytoplasmic protein p53 that regulates cell growth and death. Mutations have been identified in a variety of cancers.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> In MDS, <span class="elsevierStyleItalic">TP53</span> mutations have been found mainly in intermediate- to high-risk patients. Patients often present with complex cytogenetic abnormalities, severe thrombocytopenia, increased risk of leukemia progression, and have shorter survival.<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">7,8</span></a> While it has been well documented that genetic lesions in <span class="elsevierStyleItalic">TP53</span> carry an independent poor prognostic value, mostly amongst advanced stage patients,<a class="elsevierStyleCrossRefs" href="#bib0045"><span class="elsevierStyleSup">9,10</span></a> the role of <span class="elsevierStyleItalic">TP53</span> mutations in low-risk MDS remains unclear. Duarte et al. examined whether intracellular accumulation of mutant p53 correlates with clinical characteristics and prognosis among 38 patients with low-risk MDS (defined by current scoring system).<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Patients with mutant p53 were older, anemic and leukopenic at the time of diagnosis, and had a shorter median survival compared to those carrying wild-type p53.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Duarte et al. concluded that molecular identification of mutant p53 contributes to risk stratification of patients with low-risk MDS, which may alter the treatment approach.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> The authors provide a compelling argument for further characterization of the role of p53 in a larger cohort of low-risk MDS patients.</p><p id="par0030" class="elsevierStylePara elsevierViewall">Interpreting p53 mutation role in MDS is not a trivial task, however, since there are often complicating interactions with other intracellular regulators.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> A recent effort to characterize genetic lesions in MDS showed that each patient frequently harbors mutations in multiple genes simultaneously.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> In another study, mutations in genes <span class="elsevierStyleItalic">ASXL1</span>, <span class="elsevierStyleItalic">EZH2</span>, <span class="elsevierStyleItalic">RUNX1</span>, <span class="elsevierStyleItalic">NRAS</span> and others were associated with shorter overall survival in lower-risk MDS.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> Interestingly, interactions among these gene products and p53 have been documented extensively.<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13,14</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Over the past 5–10 years a variety of technologies have improved and enabled high-throughput analysis of entire MDS genomes, leading to the identification of several new potentially targetable genes implicated in MDS pathogenesis. The challenge is how to incorporate these into new prognostic systems. In addition, it is expected that these approaches will lead to therapeutic insights that are desperately needed for MDS patients.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0040" class="elsevierStylePara elsevierViewall">The authors declare no conflicts of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Conflicts of interest" ] 1 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:14 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Tumor suppressor p53 protein expression: prognostic significance in patients with low-risk myelodysplastic syndrome" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "F.B. 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Ano/Mês | Html | Total | |
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