Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/30123
Title: Interrelationships among chromosome aneuploidy, promoter hypermethylation, and protein expression of the CDKN2A gene in individuals from northern Brazil with gastric adenocarcinoma
Authors: Guimares, Adriana Costa
Lima, Eleonidas Moura
Khayat, Andre Salim
Henrique, Mario
Faria, Girao
Barem Rabenhorst, Silvia Helena
Ferreira, Márcia Valéria Pitombeira
Assumpcao, Paulo Pimentel
Bahia, Marcelo de Oliveira
Lima, Patricia Danielle Lima de
Cardoso Smith, Marilia de Arruda
Burbanoa, Rommel Rodriguez
Campus Univ Guama
Univ Fed Piaui
Univ Fed Ceara
Fed Univ Para
Universidade Federal de São Paulo (UNIFESP)
Issue Date: 1-Nov-2007
Publisher: Elsevier B.V.
Citation: Cancer Genetics and Cytogenetics. New York: Elsevier B.V., v. 179, n. 1, p. 45-51, 2007.
Abstract: Numerical alterations of chromosome 9, the status of promoter methylation and protein expression of the CDKN2A gene (aliases include p16 and p16(INK4a)), the possible association with gain of chromosome X, and the interrelation of these findings with clinic and pathological characteristics were investigated in gastric adenocarcinomas. Fluorescence in situ hybridization analysis with centromeric DNA probes, immunohistochemical staining, and methylation-specific polymerase chain reaction assays were performed in 15 gastric adenocarcinomas samples from individuals from northern Brazil. Aneuploidies of chromosomes X and 9 were found in all samples, both intestinal and diffuse type. Monosomy of chromosome 9 and gain of a copy of chromosome X (in both sexes) were observed in 100% of cases. Hypermethylation frequency and protein expression of CDKN2A were also found in all cases analyzed. No association of genetic and epigenetic alterations with histological type, tumor aggressiveness, and invasion was found (P > 0.05), which may be attributable to small sample size. There was a high level of association between absence of p 16 protein expression levels, CDKN2A gene promote hypermethylation, and chromosome 9 aneuploidy (100% of cases). Thus, in the present samples, the apparent mechanisms behind p16 silencing include loss of chromosome 9 and promoter region hypermethylation. (C) 2007 Elsevier Inc. All rights reserved.
URI: http://repositorio.unifesp.br/handle/11600/30123
ISSN: 0165-4608
Other Identifiers: http://dx.doi.org/10.1016/j.cancergencyto.2007.07.019
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