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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">In this issue of the Revista Brasileira de Hematologia e Hemoterapia&#44; Duarte et al&#46;<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 &#40;MDS&#41;&#46; In a cohort of 38 patients&#44; the authors demonstrated an association between mutant p53 protein expression and shortened survival&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">MDS is a clinically heterogeneous disorder&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Patients with this condition demonstrate clonal hematopoietic expansion&#44; cytopenias&#44; myelodysplasia&#44; ineffective hematopoiesis and an increased propensity to develop acute myeloid leukemia&#46; Not surprisingly&#44; prognosis is related to severity of cytopenias&#44; presence of cytogenetic abnormalities and clonal evolution demonstrated by blast counts&#44; and other &#8216;traditional&#8217; prognostic elements&#46; There is heterogeneity even among patients diagnosed with lower-risk disease&#44; since a subset of these patients have more aggressive disease&#46; Recent efforts have demonstrated that several molecular parameters linked to the pathophysiology of MDS may affect overall survival&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;4</span></a> Thus&#44; identification of additional prognosticators that more accurately characterize subgroups and their outcomes are essential&#46;</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&#40;s&#41;&#46; These mutations occur in genes encoding protein products that are involved typically in either RNA splicing or DNA methylation&#44; which in turn leads to genomic instability and further mutations&#46;<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&#46; This clone can subsequently acquire additional driver mutations that lead to the development of multiple subclonal populations&#46; The accumulation and combination of these genetic lesions likely contribute to the phenotypes observed in MDS patients&#46; <span class="elsevierStyleItalic">TP53</span> gene mutations are particularly interesting given the fact that its protein product has tumor suppression activity&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">TP53</span> encodes a cytoplasmic protein p53 that regulates cell growth and death&#46; Mutations have been identified in a variety of cancers&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> In MDS&#44; <span class="elsevierStyleItalic">TP53</span> mutations have been found mainly in intermediate- to high-risk patients&#46; Patients often present with complex cytogenetic abnormalities&#44; severe thrombocytopenia&#44; increased risk of leukemia progression&#44; and have shorter survival&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">7&#44;8</span></a> While it has been well documented that genetic lesions in <span class="elsevierStyleItalic">TP53</span> carry an independent poor prognostic value&#44; mostly amongst advanced stage patients&#44;<a class="elsevierStyleCrossRefs" href="#bib0045"><span class="elsevierStyleSup">9&#44;10</span></a> the role of <span class="elsevierStyleItalic">TP53</span> mutations in low-risk MDS remains unclear&#46; Duarte et al&#46; examined whether intracellular accumulation of mutant p53 correlates with clinical characteristics and prognosis among 38 patients with low-risk MDS &#40;defined by current scoring system&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Patients with mutant p53 were older&#44; anemic and leukopenic at the time of diagnosis&#44; and had a shorter median survival compared to those carrying wild-type p53&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Duarte et al&#46; concluded that molecular identification of mutant p53 contributes to risk stratification of patients with low-risk MDS&#44; which may alter the treatment approach&#46;<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&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Interpreting p53 mutation role in MDS is not a trivial task&#44; however&#44; since there are often complicating interactions with other intracellular regulators&#46;<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&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> In another study&#44; mutations in genes <span class="elsevierStyleItalic">ASXL1</span>&#44; <span class="elsevierStyleItalic">EZH2</span>&#44; <span class="elsevierStyleItalic">RUNX1</span>&#44; <span class="elsevierStyleItalic">NRAS</span> and others were associated with shorter overall survival in lower-risk MDS&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> Interestingly&#44; interactions among these gene products and p53 have been documented extensively&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13&#44;14</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Over the past 5&#8211;10 years a variety of technologies have improved and enabled high-throughput analysis of entire MDS genomes&#44; leading to the identification of several new potentially targetable genes implicated in MDS pathogenesis&#46; The challenge is how to incorporate these into new prognostic systems&#46; In addition&#44; it is expected that these approaches will lead to therapeutic insights that are desperately needed for MDS patients&#46;</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&#46;</p></span></span>"
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Scientific Comment
Utility of the p53 mutant protein in patients with low-risk myelodysplastic syndrome
David C. Yaoa,b, Marcos de Limaa,b,
Autor para correspondência
Marcos.deLima@uhhospitals.org

Corresponding author at: University Hospitals Case Medical Center, 11100 Euclid Avenue, Cleveland, OH 44106, United States.
a University Hospitals Case Medical Center, Cleveland, United States
b Seidman Cancer Center and Case Western Reserve University, Cleveland, United States
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    "titulo" => "Utility of the p53 mutant protein in patients with low-risk myelodysplastic syndrome"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">In this issue of the Revista Brasileira de Hematologia e Hemoterapia&#44; Duarte et al&#46;<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 &#40;MDS&#41;&#46; In a cohort of 38 patients&#44; the authors demonstrated an association between mutant p53 protein expression and shortened survival&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">MDS is a clinically heterogeneous disorder&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Patients with this condition demonstrate clonal hematopoietic expansion&#44; cytopenias&#44; myelodysplasia&#44; ineffective hematopoiesis and an increased propensity to develop acute myeloid leukemia&#46; Not surprisingly&#44; prognosis is related to severity of cytopenias&#44; presence of cytogenetic abnormalities and clonal evolution demonstrated by blast counts&#44; and other &#8216;traditional&#8217; prognostic elements&#46; There is heterogeneity even among patients diagnosed with lower-risk disease&#44; since a subset of these patients have more aggressive disease&#46; Recent efforts have demonstrated that several molecular parameters linked to the pathophysiology of MDS may affect overall survival&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;4</span></a> Thus&#44; identification of additional prognosticators that more accurately characterize subgroups and their outcomes are essential&#46;</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&#40;s&#41;&#46; These mutations occur in genes encoding protein products that are involved typically in either RNA splicing or DNA methylation&#44; which in turn leads to genomic instability and further mutations&#46;<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&#46; This clone can subsequently acquire additional driver mutations that lead to the development of multiple subclonal populations&#46; The accumulation and combination of these genetic lesions likely contribute to the phenotypes observed in MDS patients&#46; <span class="elsevierStyleItalic">TP53</span> gene mutations are particularly interesting given the fact that its protein product has tumor suppression activity&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">TP53</span> encodes a cytoplasmic protein p53 that regulates cell growth and death&#46; Mutations have been identified in a variety of cancers&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> In MDS&#44; <span class="elsevierStyleItalic">TP53</span> mutations have been found mainly in intermediate- to high-risk patients&#46; Patients often present with complex cytogenetic abnormalities&#44; severe thrombocytopenia&#44; increased risk of leukemia progression&#44; and have shorter survival&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">7&#44;8</span></a> While it has been well documented that genetic lesions in <span class="elsevierStyleItalic">TP53</span> carry an independent poor prognostic value&#44; mostly amongst advanced stage patients&#44;<a class="elsevierStyleCrossRefs" href="#bib0045"><span class="elsevierStyleSup">9&#44;10</span></a> the role of <span class="elsevierStyleItalic">TP53</span> mutations in low-risk MDS remains unclear&#46; Duarte et al&#46; examined whether intracellular accumulation of mutant p53 correlates with clinical characteristics and prognosis among 38 patients with low-risk MDS &#40;defined by current scoring system&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Patients with mutant p53 were older&#44; anemic and leukopenic at the time of diagnosis&#44; and had a shorter median survival compared to those carrying wild-type p53&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Duarte et al&#46; concluded that molecular identification of mutant p53 contributes to risk stratification of patients with low-risk MDS&#44; which may alter the treatment approach&#46;<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&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Interpreting p53 mutation role in MDS is not a trivial task&#44; however&#44; since there are often complicating interactions with other intracellular regulators&#46;<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&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> In another study&#44; mutations in genes <span class="elsevierStyleItalic">ASXL1</span>&#44; <span class="elsevierStyleItalic">EZH2</span>&#44; <span class="elsevierStyleItalic">RUNX1</span>&#44; <span class="elsevierStyleItalic">NRAS</span> and others were associated with shorter overall survival in lower-risk MDS&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> Interestingly&#44; interactions among these gene products and p53 have been documented extensively&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13&#44;14</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Over the past 5&#8211;10 years a variety of technologies have improved and enabled high-throughput analysis of entire MDS genomes&#44; leading to the identification of several new potentially targetable genes implicated in MDS pathogenesis&#46; The challenge is how to incorporate these into new prognostic systems&#46; In addition&#44; it is expected that these approaches will lead to therapeutic insights that are desperately needed for MDS patients&#46;</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&#46;</p></span></span>"
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ISSN: 15168484
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Idiomas
Hematology, Transfusion and Cell Therapy