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Epigenetic alterations of p15(INK4B) and p16(INK4A) genes in pediatric primary myelodysplastic syndrome.

Authors: Rodrigues, EF  Santos-Reboucas, CB  Goncalves Pimentel, MM  Mencalha, AL  Dobbin, J  Da Costa, ES  Fernandez Cde, S  Bouzas, LF  Abdelhay, E  De Souza Fernandez, T 
Citation: Rodrigues EF, etal., Leuk Lymphoma. 2010 Oct;51(10):1887-94. doi: 10.3109/10428194.2010.505820.
Pubmed: (View Article at PubMed) PMID:20658957
DOI: Full-text: DOI:10.3109/10428194.2010.505820

We studied the methylation status of the p15(INK4B) and p16(INK4A) genes in 47 pediatric patients with primary MDS, its correlation with subtype, and the role of p15(INK4B) and p16(INK4A) in the evolution of MDS toward AML. Aberrant methylation of the p15(INK4B) gene was detected in 15 of 47 patients (32%), whereas only four patients demonstrated methylation of the p16(INK4A) gene (8%). The frequency of p15(INK4B) methylation was significantly higher in RAEB and RAEB-t subtypes (p<0.003). Aberrant methylation of the p16(INK4A) gene was also more frequent in the subtypes that characterize advanced stages of the disease (p<0.05). Evolution of disease was verified in 17 (36%) of the 47 patients. The association of p15(INK4B) and p16(INK4A) methylation status with evolution of disease was clearly significant (p<0.008 and p<0.05, respectively). These results suggest that methylation of the p15(INK4B) and p16(INK4A) genes is an epigenetic biomarker of pediatric disease evolution.


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CRRD Object Information
CRRD ID: 11251750
Created: 2016-06-21
Species: All species
Last Modified: 2016-06-21
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.