Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/201699
Type: Artigo de periódico
Title: Ten-eleven-translocation 2 (tet2) Is Downregulated In Myelodysplastic Syndromes.
Author: Scopim-Ribeiro, Renata
Machado-Neto, João Agostinho
Campos, Paula de Melo
Silva, Cleide Aparecida Moreira
Favaro, Patricia
Lorand-Metze, Irene
Costa, Fernando Ferreira
Saad, Sara Teresinha Olalla
Traina, Fabiola
Abstract: TET2, a member of the ten-eleven-translocation (TET) family genes that modify DNA by converting 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC), is located in chromosome 4q24 and is frequently mutated in myeloid malignancies. The impact of TET2 mutation on survival outcomes is still controversial; however, functional studies have proved that it is a loss-of-function mutation that impairs myeloid cell differentiation and contributes to the phenotype of myeloid neoplasia. We, herein, aimed to investigate TET2 expression in patients with myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). A significantly decreased TET2 expression was observed in bone marrow cells from AML (n = 53) and patients with MDS (n = 64), compared to normal donors (n = 22). In MDS, TET2 expression was significantly reduced in RAEB-1/RAEB-2 compared to other WHO 2008 classifications, and a lower TET2 expression was observed at the time of MDS disease progression in four of five patients. In multivariate analysis, low TET2 expression (P = 0.03), male gender (P = 0.02), and WHO 2008 classification (P < 0.0001) were independent predictors of poorer overall survival. These results suggest that defective TET2 expression plays a role in the MDS pathophysiology and predicts survival outcomes in this disease.
Subject: Acute Myeloid Leukemia
Myelodysplastic Syndromes
Ten-eleven-translocation 2
Rights: fechado
Identifier DOI: 10.1111/ejh.12445
Address: http://www.ncbi.nlm.nih.gov/pubmed/25200248
Date Issue: 2014
Appears in Collections:Artigos e Materiais de Revistas Científicas - Unicamp

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