Quantitative analysis of CDKN2A methylation, mRNA, and p16(INK4a) protein expression in children and adolescents with Burkitt lymphoma: biological and clinical implications.

Autor: Robaina MC; Programa de Pesquisa em Hemato-Oncologia Molecular, Instituto Nacional de Câncer, Rio de Janeiro, Brazil., Faccion RS; Programa de Pesquisa em Hemato-Oncologia Molecular, Instituto Nacional de Câncer, Rio de Janeiro, Brazil., Arruda VO; Programa de Pesquisa em Hemato-Oncologia Molecular, Instituto Nacional de Câncer, Rio de Janeiro, Brazil., de Rezende LM; Divisão de Patologia, Instituto Nacional de Câncer, Rio de Janeiro, Brazil., Vasconcelos GM; Programa de Hematologia e Oncologia Pediátrica, Instituto Nacional de Câncer, Rio de Janeiro, Brazil., Apa AG; Serviço de Hematologia, Instituto Nacional de Câncer, Rio de Janeiro, Brazil., Bacchi CE; Consultoria em Patologia, Botucatu, São Paulo, Brazil., Klumb CE; Programa de Pesquisa em Hemato-Oncologia Molecular, Instituto Nacional de Câncer, Rio de Janeiro, Brazil. Electronic address: cklumb@inca.gov.br.
Jazyk: angličtina
Zdroj: Leukemia research [Leuk Res] 2015 Feb; Vol. 39 (2), pp. 248-56. Date of Electronic Publication: 2014 Dec 09.
DOI: 10.1016/j.leukres.2014.11.023
Abstrakt: CDKN2A is a tumor suppressor gene critical in the cell cycle regulation. Little is known regarding the role of CDKN2A methylation in the pathogenesis of Burkitt lymphoma (BL). CDKN2A methylation was investigated using pyrosequencing in 51 tumor samples. p16(INK4a) mRNA and protein levels were measured using real-time PCR and immunohistochemistry, respectively. CDKN2A methylation was detectable in 72% cases. Nuclear expression of p16(INK4a) was not detected in 41% cases. There was an association between methylation and absence of CDKN2A mRNA (P=0.003). In conclusion, CDKN2A methylation occurs at a high frequency suggesting a role in BL pathogenesis and potential therapeutic implications.
(Copyright © 2014 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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